Breast cancer (BC) has become the most common malignant tumor in women worldwide. This study was carried out to find and validate a novel molecular therapeutic target for BC.

Long non-coding RNA (lncRNA) AK023507 was selected as the study objects through microarray analysis. The function of lncRNA AK023507 was verified by various cell function experiments in vitro, subcutaneous tumorigenesis experiments, and lung metastasis model experiments in vivo. The RNA pull-down experiment and Western blot experiment were used to confirm the mechanism regulation pathway and the recovery experiment was used to verify it. TCGA datasets were used for clinical and immune function prediction analysis.

In vitro cell function tests and in vivo experiments suggested that overexpression of lncRNA AK023507 inhibited the proliferation and metastasis of BC cells. The RNA pull-down experiment and Western blot analysis validated that lncRNA AK023507 interacted with the dedicator of cytokinesis 4 (DOCK4) protein. Analysis of public databases predicted that DOCK4 is a potential prognostic risk factor associated with epithelial-mesenchymal transition (EMT) and central memory T cell (TCM) cellular immune infiltration.

LncRNA AK023507 inhibits the proliferation and metastasis of BC by regulating the DOCK4/β-catenin axis. This discovery will provide new potential therapeutic targets for BC.

Osteosarcoma is one of the most common malignant tumors in children and adolescents. It occurs in the metaphysis of long bones and is a type of aggressive malignant tumor. Although there are treatment methods such as surgery and chemotherapy, the mortality and disability of osteosarcoma patients are still high. With the emergence of more and more chemotherapy resistance, it is necessary to find new therapies to improve the chemotherapy sensitivity of osteosarcoma.

Drug-resistant MG-63 and U2OS cell strain was established in vitro by continuous exposure of human osteosarcoma cells to doxorubicin at gradually increasing concentrations，then determined for resistance index to doxorubicin by MTT method，for transcriptions of Livin mRNA by real-time polymerase chain reaction（RT⁃PCR），and for expressions of Livin proteins by Western blot．The technology of gene recombination was used to construct the eukaryotic expression vector pSilencer3.1-H1 neo-Livin. Then the pSilencer3.1-H1 neo-Livin was transfected into drug-resistant MG-63 cell by using Lipofectmine 2000. Expressions of Livin mRNA and protein in the transfected cells were respectively measured by RT-PCR and Western blot. The distribution of cell cycle phase and apoptosis were determined by flow cytometry. The analysis of chemotherapeutic sensitivity of drug-resistant MG-63 cell to doxorubicin was performed by MTT.

The recombinant eukaryotic expression vector pSilencer3.1-H1 neo-Livin was successfully constructed. The result of inverted microscope revealed that the drug-resistant MG-63 cell were irregularity and morphological diversity. Compared with those in osteosarcoma cells，the transcription levels of Livin mRNA and protein in drug-resistant osteosarcoma cell increased（P＜0.05）．The flow cytometry analysis showed there was higher percentage of apoptosis in transfected drug-resistant MG-63 cell. Compared with control groups，the expression of Livin mRNA and protein were both significantly decreased in the transfected drug-resistant osteosarcomacell（P＜0.05）. We also observed that suppression of Livin expression in osteosarcoma cells increased their chemosensitivity to doxorubicin.

This study showed that Livin shRNA inhibited the proliferation level and increased the sensitivity of drug-resistant osteosarcoma cell to doxorubicin, suggested that Livin is involved in drug resistance of human osteosarcoma and may serve as a promising therapeutic target for osteosarcoma.

Starvation stress is one of the most common environmental challenges faced by aquatic animals, often leading to compensatory growth, a widespread phenomenon in the animal kingdom, especially among aquatic species. The sea cucumber (Apostichopus japonicus), a key marine economic species in China, has been shown to utilize long non-coding RNAs (lncRNAs) in responding to environmental changes, pathogen infections, and tissue regeneration. In this study, strand-specific high-throughput sequencing was employed to analyze transcriptomic data from degenerated intestines of A. japonicus under starvation conditions. High-quality lncRNAs were identified and classified, and key differentially expressed mRNAs and lncRNAs associated with intestinal degradation were screened. A gene interaction network model based on the competing endogenous RNA (ceRNA) theory was then constructed. The analysis revealed that the "AjSOX9/Aja-miR-2012-5p/MSTRG.2956.1 and MSTRG.5699.1" axes, as well as the "AjWNT9B/Aja-miR-200-3p/MSTRG.19757.1 and MSTRG.21788.1" axes, play significant roles in degraded intestines and may promote intestinal regeneration during compensatory growth. Additionally, the "AjFABP2/Aja-miR-9-5p/MSTRG.9667.1" axis appears to regulate energy metabolism under starvation stress. These findings provide valuable insights into the non-coding gene regulatory networks in invertebrates under starvation stress and offer a scientific foundation for developing stress-resistant sea cucumber strains, contributing to the sustainable development of the sea cucumber aquaculture industry.

Prostate cancer (PCa) is a leading cause of cancer-related morbidity and mortality in men worldwide. Despite advancements in diagnosis and treatment, challenges such as late-stage detection, therapeutic resistance, and the complexity of castration-resistant prostate cancer (CRPC) persist. Long non-coding RNAs (LncRNAs) play critical roles in PCa progression through epigenetic regulation, transcriptional and post-transcriptional modulation, and immune response regulation. This review highlights the molecular mechanisms by which LncRNAs influence PCa development, treatment resistance, and immune regulation, emphasizing their potential as biomarkers and therapeutic targets. We also discuss future research directions to advance precision medicine in PCa.

Background: Disulfide-dependent cell death, known as disulfide death, plays a pivotal regulatory role in the onset and progression of various cancers including pancreatic cancer. Despite its significance, little attention has been given to the study of disulfide death-related long non-coding RNAs (lncRNAs) in pancreatic cancer development and progression. Methods: This study utilized data from the Cancer Genome Atlas Project (TCGA) to analyze the transcriptome of pancreatic cancer. Co-expression analysis of genes associated with disulfide death was performed and six lncRNAs closely linked to disulfide death were identified through univariate and multivariate analysis. These lncRNAs were used to develop clinical prognostic models. The prognostic value of this model was then analyzed and further investigations included pathway enrichment analysis, tumor mutation load analysis, immune cell infiltration analysis, analysis of the tumor microenvironment (TME), and drug sensitivity analysis. Results: The developed prognostic model based on disulfide-associated lncRNAs exhibited significant prognostic value, allowing for reliable predictions of patient outcomes in pancreatic adenocarcinoma (PAAD). The analysis revealed that the six identified lncRNAs serve as independent prognostic factors, significantly correlating with patient survival and recurrence rates. Additionally, findings indicated notable differences in immune cell infiltration and drug sensitivity between high-risk and low-risk patient groups, suggesting potential therapeutic targets for enhancing treatment efficacy. Conclusions: Our findings revealed six disulfide death-associated lncRNAs with independent prognostic value, offering a crucial indicator for predicting the prognosis of pancreatic adenocarcinoma (PAAD) patients. Additionally, the analysis of tumor immune invasion and drug sensitivity provides a novel avenue for controlling tumor invasion and metastasis as well as reducing drug tolerance.

Fat deposition represents a crucial feature in the expenditure of physical energy and affects the meat quality of farm animals. It is regulated by multiple genes and regulators. Of them, non-coding RNAs (ncRNAs) play a critical role in modulating the fat deposition process. As well as being an important protein source, farm animals can be used as medical models, so many researchers worldwide have explored their mechanism of fat deposition. This article summarizes the transcription factors, regulatory genes, and signaling pathways involved in the molecular regulation process of fat deposition; outlines the progress of researching the roles of microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs) in fat deposition in common farm animals including pigs, cattle, sheep, ducks, and chickens; and identifies scientific problems in the field that must be further investigated. It has been demonstrated that ncRNAs play a critical role in regulating the fat deposition process and have great potential in improving meat quality traits.

Long non-coding RNAs (lncRNAs) play diverse biological roles within cells. Despite not encoding proteins, they are crucial in regulating gene expression, chromatin structure and function, cell differentiation and development, and the occurrence of diseases. Vibrio alginolyticus (V. alginolyticus) is a common bacterium found in marine environments that poses a threat to shellfish by infecting them through filtration feeding. Research has demonstrated the substantial involvement of lncRNAs in the immune response of shellfish. However, the specific mechanism by which lncRNAs participate in the immune regulatory process following infection of Mytilus coruscus (M. coruscus) with V. alginolyticus has not been investigated. Therefore, the transcription profiles of lncRNAs in M. coruscus hemocytes were investigated. A grand total of 48,246 lncRNAs were detected, with 2421 genes that exhibited and 717 lncRNAs that had differential expression. To gain a better understanding of the potential roles of the differentially expressed lncRNAs (DE-lncRNAs), GO and KEGG pathway analyses were performed on their target mRNAs, suggesting that lncRNAs have the ability to control gene expression levels and consequently influence immune-related pathways, hence regulating the immune response in M. coruscus. Additionally, a total of 138 lncRNA-mRNA pairs were identified through the calculation of co-expression relationships between DE-lncRNAs and immune-related DE-mRNAs. These findings provide new insights into the role of lncRNAs in the immune response of M. coruscus and offer important resources for further investigation into the role of lncRNAs in M. coruscus pathogen infection.

Osteosarcoma (OS) is the most common bone malignancy in children and adolescents, and although current neoadjuvant chemotherapy has shown efficacy against OS, the long-term survival rate for patients with OS remains low, highlighting the need to find more effective treatments. In cancer cells, abnormal activation of signaling pathways can widely affect cell activity from growth and proliferation to apoptosis, invasion and metastasis. Wnt/β-catenin is a complex and unique signaling pathway that is considered to be one of the most important carcinogenic pathways in human cancer. Research have confirmed that the Wnt/β-catenin signaling pathway is an important driving factor for the occurrence and development of osteosarcoma, and abnormal activation of this pathway can promote the pathological processes of cell proliferation, invasion, migration, tumor angiogenesis and chemical resistance of osteosarcoma. However, inhibition of Wnt/β-catenin signaling pathway can effectively inhibit or reverse the above pathological processes. Therefore, manipulating the expression or function of the Wnt/β-catenin pathway may be a potential targeted pathway for the treatment of OS. In this review, we describe the characteristics of the Wnt/β-catenin signaling pathway and summarize the role and mechanism of this pathway in OS. This paper discusses the therapeutic significance of inhibiting or targeting Wnt/β-catenin pathway in OS and the shortcomings of current studies on this pathway in OS and the problems to be solved. This review helps us to understand the role of Wnt/β-catenin on OS, and provides a theoretical basis and new ideas for targeting Wnt/β-catenin pathway as a therapeutic target for OS.

(Tumor-educated platelets) TEPs have emerged as active players in all steps of tumorigenesis, confrontation of platelets with tumor cells via transfer of tumor-associated biomolecules and results in the sequestration of such biomolecules. The current study was aimed to examine whether TEPs lncRNA-STARD4-AS1 and ELOA-AS1 might be potential biomarkers for NSCLC.

TEPs were obtained by low-speed centrifugation. Quantitative real-time PCR was used to determine the expression level of TEPs-STARD4-AS1, ELOA-AS1 in the training cohort and the validation cohort. ROC curve was generated to evaluate their diagnostic value. Correlations between TEPs-STARD4-AS1, ELOA-AS1 and clinical parameters were further analyzed.

Our results showed that the level of TEPs-STARD4-AS1 and ELOA-AS1 significantly upregulated in patients with NSCLC compared with healthy controls in the two cohorts. By ROC analysis, we found that TEPs-STARD4-AS1, ELOA-AS1 could offer valuable diagnostic performance for NSCLC patients (AUCSTARD4-AS1 = 0.800/0.774, and AUCELOA-AS1 = 0.754/0.718 for diagnosing adenocarcinoma and squamous cell carcinoma cases from controls, respectively). The combination of TEP-STARD4-AS1 and ELOA-AS1 improved the diagnostic efficiency of NSCLC. Clinicopathological analysis further revealed that TEPs-STARD4-AS1 level significantly correlated with tumor-node-metastasis (TNM) stage (p = 0.011), while TEPs-ELOA-AS1 expression significantly correlated with tumor-node-metastasis (TNM) stage and (p = 0.019) distant metastasis (p = 0.004).

Our data suggested that TEPs-STARD4-AS1 and ELOA-AS1 are promising non-invasive circulating diagnostic markers for NSCLC.

The mostly aggressive and extremely malignant type of central nervous system is Glioblastoma (GBM), which is characterized by an extremely short average survival time of lesser than 16 months. The primary cause of this phenomenon can be attributed to the extensively altered genome of GBM, which is characterized by the dysregulation of numerous critical signaling pathways and epigenetics regulations associated with proliferation, cellular growth, survival, and apoptosis. In light of this, different genetic alterations in critical signaling pathways and various epigenetics regulation mechanisms are associated with GBM and identified as distinguishing markers. Such GBM prognostic alterations are identified in PI3K/AKT, p53, RTK, RAS, RB, STAT3 and ZIP4 signaling pathways, metabolic pathway (IDH1/2), as well as alterations in epigenetic regulation genes (MGMT, CDKN2A-p16INK4aCDKN2B-p15INK4b). The exploration of innovative diagnostic and therapeutic approaches that specifically target these pathways is utmost importance to enhance the future medication for GBM. This study provides a comprehensive overview of dysregulated epigenetic mechanisms and signaling pathways due to mutations, methylation, and copy number alterations of in critical genes in GBM with prevalence and emphasizing their significance.

Melanoma is an aggressive tumor with a high mortality rate. Metformin, a commonly prescribed diabetes medication, has shown promise in cancer prevention and treatment. Long noncoding RNAs (lncRNAs) are non-protein-coding RNA molecules that play a key role in tumor development by interacting with cellular chromatins. Despite the benefits of metformin, the anticancer mechanism underlying its effect on the regulation of lncRNAs in melanoma remains unclear.

We investigated the lncRNA profiles of human melanoma cells with and without metformin treatment using a next-generation sequencing approach (NGS). Utilizing public databases, we analyzed the expression levels and clinical impacts of LINC00094 and miR-1270 in melanoma. The expression levels of LINC00094 and miR-1270 were verified in human cell lines and clinical samples by real-time PCR and in situ hybridization. The biological roles of LINC00094 and miR-1270 in cell growth, proliferation, cell cycle, apoptosis, and motility were studied using in vitro assays.

We identify a novel long noncoding RNA, namely LINC00094, whose expression considerably decreased in melanoma cells after metformin treatment. In situ hybridization analysis revealed substantially higher expression of LINC00094 in cutaneous melanoma tissue compared with adjacent normal epidermis and normal control tissues (P < 0.001). In nondiabetic patients with melanoma, the overall survival of high LINC00094 expression group was shorter than the low LINC00094 expression group with borderline statistical significance (log-rank test, P = 0.057). Coexpression analysis of LINC00094 indicated its involvement in the mitochondrial respiratory pathway, with its knockdown suppressing genes associated with mitochondrial oxidative phosphorylation, glycolysis, antioxidant production, and metabolite levels. Functional analysis revealed that silencing-LINC00094 inhibited the proliferation, colony formation, invasion, and migration of melanoma cells. Cell cycle analysis following LINC00094 knockdown revealed G1 phase arrest with reduced cell cycle protein expression. Combined TargetScan and reporter assays revealed a direct link between miR-1270 and LINC00094. Ectopic miR-1270 expression inhibited melanoma cell growth and motility while inducing apoptosis. Finally, through in silico analysis, we identified two miR-1270 target genes, CD276 and centromere protein M (CENPM), which may be involved in the biological functions of LINC00094.

Overall, LINC00094 expression may regulate melanoma cell growth and motility by modulating the expression of miR-1270, and targeting genes of CD276 and CENPM indicating its therapeutic potential in melanoma treatment.

Periodontitis can lead to the destruction of periodontal tissues and potentially tooth loss. Numerous periodontal tissue-derived cells display osteogenic differentiation potential. The presence of differentially expressed long non-coding RNAs (lncRNAs) in these cells indicate their ability to regulate the process of osteogenic differentiation. We aim to elucidate the various lncRNA-mediated regulatory mechanisms in the osteogenic differentiation of periodontal tissue-derived cells in the field of periodontitis at epigenetic modification, transcriptional, and post-transcriptional levels.

We systematically searched the PubMed, Web of Science, and ScienceDirect databases to identify relevant literature in the field of periodontitis discussing the role of lncRNAs in regulating osteogenic differentiation of periodontal tissue-derived cells. The identified literature was subsequently summarized for comprehensive review.

In this review, we have comprehensively summarized the regulatory mechanisms of lncRNAs in the osteogenic differentiation of periodontal tissue-derived cells in the field of periodontitis and discussed how these lncRNAs provide novel perspectives for understanding the pathogenesis and progression of periodontitis.

These results indicate the pivotal role of lncRNAs as regulators in the osteogenic differentiation of periodontal tissue-derived cells, providing a solid basis for future investigations on the role of lncRNAs in the periodontitis field.

Long non-coding RNAs (lncRNAs) play crucial roles in the regulation of gene expression and maintenance of genomic integrity through various interactions with DNA, RNA, and proteins. The availability of large-scale sequence data from various high-throughput platforms has opened possibilities to identify, predict, and functionally annotate lncRNAs. As a result, there is a growing demand for an integrative computational framework capable of identifying known lncRNAs, predicting novel lncRNAs, and inferring the downstream regulatory interactions of lncRNAs at the genome-scale. We present ETENLNC (End-To-End-Novel-Long-NonCoding), a user-friendly, integrative, open-source, scalable, and modular computational framework for identifying and analyzing lncRNAs from raw RNA-Seq data. ETENLNC employs six stringent filtration steps to identify novel lncRNAs, performs differential expression analysis of mRNA and lncRNA transcripts, and predicts regulatory interactions between lncRNAs, mRNAs, miRNAs, and proteins. We benchmarked ETENLNC against six existing tools and optimized it for desktop workstations and high-performance computing environments using data from three different species. ETENLNC is freely available on GitHub: https://github.com/EvolOMICS-TU/ETENLNC.

The development of endometrial receptivity is crucial for successful embryo implantation and the initiation of pregnancy. Understanding the molecular regulatory processes that transform the endometrium into a receptive phase is essential for enhancing implantation rates in fertility treatments, such as in vitro fertilization (IVF). Long non-coding RNAs (lncRNAs) play a pivotal role as gene regulators and have been examined in the endometrium. This review offers current insights into the role of lncRNAs in regulating endometrial receptivity. Considering the significant variation in endometrial remodeling among species, we summarize the key events in the human endometrial cycle and discuss the identified lncRNAs in both humans and other species, which may play a crucial role in establishing receptivity. Notably, there are 742 lncRNAs in humans and 4438 lncRNAs that have the potential to modulate endometrial receptivity. Additionally, lncRNAs regulating matrix metalloproteinases (MMPs) and Let-7 have been observed in both species. Future investigations should explore the potential of lncRNAs as therapeutic targets and/or biomarkers for diagnosing and improving endometrial receptivity in human fertility therapy.

Virus‒host protein‒lncRNA interaction (VHPLI) predictions are critical for decoding the molecular mechanisms of viral pathogens and host immune processes. Although VHPLI interactions have been predicted in both plants and animals, they have not been extensively studied in viruses. For the first time, we propose a new deep learning-based approach that consists mainly of a convolutional neural network and bidirectional long and short-term memory network modules in combination with transfer learning named CBIL‒VHPLI to predict viral-host protein‒lncRNA interactions. The models were first trained on large and diverse datasets (including plants, animals, etc.). Protein sequence features were extracted using a k-mer method combined with the one-hot encoding and composition-transition-distribution (CTD) methods, and lncRNA sequence features were extracted using a k-mer method combined with the one-hot encoding and Z curve methods. The results obtained on three independent external validation datasets showed that the pre-trained CBIL‒VHPLI model performed the best with an accuracy of approximately 0.9. Pretraining was followed by conducting transfer learning on a viral protein-human lncRNA dataset, and the fine-tuning results showed that the accuracy of CBIL‒VHPLI was 0.946, which was significantly greater than that of the previous models. The final case study results showed that CBIL‒VHPLI achieved a prediction reproducibility rate of 91.6% for the RIP-Seq experimental screening results. This model was then used to predict the interactions between human lncRNA PIK3CD-AS2 and the nonstructural protein 1 (NS1) of the H5N1 virus, and RNA pull-down experiments were used to prove the prediction readiness of the model in terms of prediction. The source code of CBIL‒VHPLI and the datasets used in this work are available at https://github.com/Liu-Lab-Lnu/CBIL-VHPLI for academic usage.

Hepatocellular carcinoma (HCC) is a primary contributor to cancer-related mortality on a global scale. However, the underlying molecular mechanisms are still poorly understood. Long noncoding RNAs are emerging markers for HCC diagnosis, prognosis, and therapeutic target. No study of LINC01767 in HCC was published.

To conduct a multi-omics analysis to explore the roles of LINC01767 in HCC for the first time.

DESeq2 Package was used to analyze different gene expressions. Receiver operating characteristic curves assessed the diagnostic performance. Kaplan-Meier univariate and Cox multivariate analyses were used to perform survival analysis. The least absolute shrinkage and selection operator (LASSO)-Cox was used to identify the prediction model. Subsequent to the validation of LINC01767 expression in HCC fresh frozen tissues through quantitative real time polymerase chain reaction, next generation sequencing was performed following LINC01767 over expression (GSE243371), and Gene Ontology/Kyoto Encyclopedia of Genes and Genomes/Gene Set Enrichment Analysis/ingenuity pathway analysis was carried out. In vitro experiment in Huh7 cell was carried out.

LINC01767 was down-regulated in HCC with a log fold change = 1.575 and was positively correlated with the cancer stemness. LINC01767 was a good diagnostic marker with area under the curve (AUC) [0.801, 95% confidence interval (CI): 0.751-0.852, P = 0.0106] and an independent predictor for overall survival (OS) with hazard ratio = 1.899 (95%CI: 1.01-3.58, P = 0.048). LINC01767 nomogram model showed a satisfied performance. The top-ranked regulatory network analysis of LINC01767 showed the regulation of genes participating various pathways. LASSO regression identified the 9-genes model showing a more satisfied performance than 5-genes model to predict the OS with AUC > 0.75. LINC01767 was down-expressed obviously in tumor than para-tumor tissues in our cohort as well as in cancer cell line; the over expression of LINC01767 inhibit cell proliferation and clone formation of Huh7 in vitro.

LINC01767 was an important tumor suppressor gene in HCC with good diagnostic and prognostic performance.

Increasing evidence has underscored the role of long noncoding RNAs (lncRNAs) make up the major proportion of the competing endogenous RNAs (ceRNAs) network and can regulate gene expression by competitively binding to miRNAs in the development and progression of tumors. Nevertheless, the role of lncRNA-mediated ceRNAs in gastric cancer (GC) and their regulatory mechanisms have not been elucidated to some extent. This study is aimed at constructing a prognostic risk model for GC based on lncRNAs. A TCGA (The Cancer Genome Atlas) dataset was analyzed using edgeR to identify differentially expressed lncRNAs (DElncRNAs) in GC tissues vs normal tissues. Subsequently, DElncRNAs that could predict GC prognosis were determined using a training set. A prognostic risk model based on the DElncRNAs was then constructed. The performance of the model was tested using a test set. The functions of these lncRNAs in GC were investigated using a lncRNA-miRNA-mRNA network. Analysis of lncRNA expression in 407 TCGA GC cases identified 3 lncRNAs that significantly correlated with prognosis. GC cases with high-risk scores showed markedly poor prognosis relative to those with low-risk scores in both the training and test sets. Univariate and multivariate Cox regression analysis of the relationship between various clinical features and prognosis found that these lncRNAs and stage significantly correlated with GC prognosis. A lncRNA-miRNA-mRNA network based on 3 lncRNAs and functional enrichment analysis of interacting mRNA indicated that these genes are enriched in various intracellular receptor signaling pathways, including regulation of muscle system process, and protein deubiquitylation. The current study provides novel insights into the lncRNA-related ceRNA network in GC and sheds lights on underlying 3 lncRNA biomarkers may be independent prognostic signatures in predicting the survival of GC patients.

This study aimed to examine the role of long non-coding RNA PCED1B antisense RNA 1 (PCED1B-AS1) in the development of hepatocellular carcinoma (HCC).

A total of 62 pairs of HCC tissues and adjacent non-tumor tissues were obtained from 62 HCC patients. The interactions of PCED1B-AS1 and microRNA-34a (miR-34a) were detected by dual luciferase activity assay and RNA pull-down assay. The RNA expression levels of PCED1B-AS1, miR-34a and CD44 were detected by RT-qPCR, and the protein expression level of CD44 was determined by Western blotting. The cell proliferation was detected by cell proliferation assay, and the cell invasion and migration by transwell invasion assay. The HCC tumor growth after PCED1B-AS1 was downregulated was determined by in vivo animal study.

PCED1B-AS1 was highly expressed in HCC tissues, which was associated with poor survival of HCC patients. Furthermore, PCED1B-AS1 interacted with miR-34a in HCC cells, but they did not regulate the expression of each other. Additionally, PCED1B-AS1 increased the expression level of CD44, which was targeted by miR-34a. The cell proliferation and invasion assay revealed that miR-34a inhibited the proliferation and invasion of HCC in vitro, while CD44 exhibited the opposite effects. Furthermore, PCED1B-AS1 suppressed the role of miR-34a. Moreover, the knockdown of PCED1B-AS1 repressed the HCC tumor growth in nude mice in vivo.

PCED1B-AS1 may play an oncogenic role by regulating the miR-34a/CD44 axis in HCC.

Colorectal cancer (CRC) is a major worldwide health issue, with high rates of both occurrence and mortality. Dysregulation of the transforming growth factor-beta (TGF-β) signaling pathway is recognized as a pivotal factor in CRC pathogenesis. Notably, the INHBA gene and long non-coding RNAs (lncRNAs) have emerged as key contributors to CRC progression. The aim of this research is to explore the immunological roles of INHBA and PELATON in CRC through a combination of computational predictions and experimental validations, with the goal of enhancing diagnostic and therapeutic strategies. In this study, we utilized bioinformatics analyses, which involved examining differential gene expression (DEG) in the TCGA-COAD dataset and exploring the INHBA gene in relation to the TGF-β pathway. Additionally, we analyzed mutations of INHBA, evaluated the microenvironment and tumor purity, investigated the INHBA's connection to immune checkpoint inhibitors, and measured its potential as an immunotherapy target using the TIDE score. Utilizing bioinformatics analyses of the TCGA-COAD dataset beside experimental methodologies such as RT-qPCR, our investigation revealed significant upregulation of INHBA in CRC. As results, our analysis of the protein-protein interaction network associated with INHBA showed 10 interacting proteins that play a role in CRC-associated processes. We observed a notable prevalence of mutations within INHBA and explored its correlation with the response to immune checkpoint inhibitors. Our study highlights INHBA as a promising target for immunotherapy in CRC. Moreover, our study identified PELATON as a closely correlated lncRNA with INHBA, with experimental validation confirming their concurrent upregulation in CRC tissues. Thus, these findings highlight the importance of INHBA and PELATON in driving CRC progression, suggesting their potential utility as diagnostic and prognostic biomarkers. By integrating computational predictions with experimental validations, this research enhances our understanding of CRC pathogenesis and uncovers prospects for personalized therapeutic interventions.

Lung cancer is one of the commonest cause of cancer associated mortality worldwide. Platelets have emerged as key players in cancer development and progression by supporting tumor growth, and dissemination. In the present systematic review, we analyzed RNA transfer between cancer cells and platelets and explored potential role of different platelet RNA profiles as onco-signature in diagnosis, subtyping, disease progression and treatment monitoring in carcinoma lung carcinoma.

The study followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and Cochrane Manual of Systematic Reviews and Meta-analysis that included seven studies on patients with lung cancer, with data on tumor-educated platelets, and control group. The outcome measured was based on sensitivity, specificity, and ROC. PUBMED, SCOPUS, Central Cochrane Registry of Controlled Trials and Science Direct databases were searched using specific search terms until October 2023. QUADAS - 2 tool was used to assess quality, risk of bias and applicability concerns.

The analysis revealed AUC > 70% for different platelet mRNAs, with sensitivity and specificity of more than 60 %. AUC and sensitivity were highest for ITGA2B (AUC 0.922; sensitivity 92.8%). lncRNA GTF2H2-1 was the most specific platelet RNA. On QUADAS-2 tool, 3/7 articles were unclear in reference standards, patient flow timing, and 1/7 had high bias in both aspects. For applicability, 1/7 studies were unclear in reference standards, and 2/7 in index tests.

TEP RNA can aid in early diagnosis of lung cancer and of proven utility in its early-stage detection. TEP RNA can also monitor disease progression and treatment response.

Acute lymphoblastic leukemia (ALL) is the most prevailing cancer among children. Despite extensive studies, ALL etiology is still an unsolved puzzle. Long non-coding RNAs (lncRNAs) emerged as key mediators in cancer etiology. Several lncRNAs are dysregulated in ALL, leading to oncogenic or tumor-suppressive activities. Additionally, a relation between ABO blood groups and hematological malignancies was proposed. The current study intended to explore the association of lncRNAs, ANRIL and LINC-PINT, and their downstream targets, CDKN2A and heme oxygenase-1 (HMOX1), with the incidence of ALL and treatment response, and to determine the distribution of blood groups across different childhood ALL phenotypes. Blood samples were taken from 66 ALL patients (at diagnosis and at the end of remission induction phase) and 39 healthy children. Whole blood was used for blood group typing. Expression of ANRIL, LINC-PINT and CDKN2A was analyzed in plasma by qRT-PCR. Serum HMOX1 was measured using ELISA. ANRIL and CDKN2A were upregulated, while LINC-PINT and HMOX1 were downregulated in newly diagnosed patients. All of which showed remarkable diagnostic performance, where HMOX1 was superior. HMOX1 was independent predictor of ALL as well. LINC-PINT and HMOX1 were significantly upregulated after treatment. Notably, ANRIL and LINC-PINT were associated with poor outcome. No significant difference in the distribution of ABO blood groups was observed between patients and controls. In conclusion, our results suggested an association of ANRIL and LINC-PINT with childhood ALL predisposition, at least in part, through altering CDKN2A and HMOX1 production. Furthermore, the impact of remission induction treatment was newly revealed.

The objective of this study was to investigate the involvement of the long non-coding RNA (lncRNA) BRE-AS1 in clear cell renal cell carcinoma (ccRCC) and to explore its potential therapeutic role.

The expression of BRE-AS1 and miR-106b-5p was determined by qRT-PCR. Overexpression of BRE-AS1 and miR-106b-5p were performed to study their relationship. Transwell assays were used to evaluate cell movement. Methylation-specific PCR (MSP) was performed to explore the role of BRE-AS1 in the methylation of the miR-106b-5p gene.

The results showed that the expression levels of BRE-AS1 were decreased, while those of miR-106b-5p were increased in ccRCC tissues. BRE-AS1 was found to be closely associated with the prognosis of patients with ccRCC. The expression of BRE-AS1 was inversely correlated with that of miR-106b-5p in tumor tissues. Overexpression of BRE-AS1 led to decreased expression levels of miR-106b-5p and increased methylation of the miR-106b-5p gene, whereas miR-106b-5p did not affect the expression of BRE-AS1. BRE-AS1 inhibited the movement and proliferation of ccRCC cell lines, while miR-106b-5p suppressed the role of BRE-AS1.

BRE-AS1 may suppress ccRCC by downregulating the expression of miR-106b-5p.

Cancer cells employ adaptive mechanisms to survive various stressors, including genotoxic drugs. Understanding the factors promoting survival is crucial for developing effective treatments. In this study, we unveil a previously unexplored long non-coding RNA, JUNI (JUN-DT, LINC01135), which is upregulated by genotoxic drugs through the activation of stress-activated MAPKs, JNK, and p38 and consequently exerts positive control over the expression of its adjacent gene product c-Jun, a well-known oncoprotein, which transduces signals to multiple transcriptional outputs. JUNI regulates cellular migration and has a crucial role in conferring cellular resistance to chemotherapeutic drugs or UV radiation. Depletion of JUNI markedly increases the sensitivity of cultured cells and spheroids to chemotherapeutic agents. We identified 57 proteins interacting with JUNI. The activity of one of them the MAPK phosphatase and inhibitor, DUSP14, is counteracted by JUNI, thereby, facilitating efficient JNK phosphorylation and c-Jun induction when cells are exposed to UV radiation. The antagonistic interplay with DUSP14 contributes not only to c-Jun induction but also augments the survival of UV-exposed cells. In summary, we introduce JUNI as a novel stress-inducible regulator of c-Jun, positioning it as a potential target for enhancing the sensitivity of cancer cells to chemotherapy.

Predicting disease-related microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) is crucial to find new biomarkers for the prevention, diagnosis, and treatment of complex human diseases. Computational predictions for miRNA/lncRNA-disease associations are of great practical significance, since traditional experimental detection is expensive and time-consuming. In this paper, we proposed a consensual machine-learning technique-based prediction approach to identify disease-related miRNAs and lncRNAs by high-order proximity preserved embedding (HOPE) and eXtreme Gradient Boosting (XGB), named HOPEXGB. By connecting lncRNA, miRNA, and disease nodes based on their correlations and relationships, we first created a heterogeneous disease-miRNA-lncRNA (DML) information network to achieve an effective fusion of information on similarities, correlations, and interactions among miRNAs, lncRNAs, and diseases. In addition, a more rational negative data set was generated based on the similarities of unknown associations with the known ones, so as to effectively reduce the false negative rate in the data set for model construction. By 10-fold cross-validation, HOPE shows better performance than other graph embedding methods. The final consensual HOPEXGB model yields robust performance with a mean prediction accuracy of 0.9569 and also demonstrates high sensitivity and specificity advantages compared to lncRNA/miRNA-specific predictions. Moreover, it is superior to other existing methods and gives promising performance on the external testing data, indicating that integrating the information on lncRNA-miRNA interactions and the similarities of lncRNAs/miRNAs is beneficial for improving the prediction performance of the model. Finally, case studies on lung, stomach, and breast cancers indicate that HOPEXGB could be a powerful tool for preclinical biomarker detection and bioexperiment preliminary screening for the diagnosis and prognosis of cancers. HOPEXGB is publicly available at https://github.com/airpamper/HOPEXGB.

In several forms of malignant tumors, nuclear enriched abundant transcript 1 (NEAT1), a lncRNA, has been identified to play an important role. NEAT1's regulation patterns in prostate cancer (PCa) are, however, mainly unknown. This study was aimed to evaluate and study the roles and regulatory mechanisms of NEAT1 in PCa. NEAT1, miR-582-5p, and enhancer of zeste homolog 2 (EZH2) expression were detected by qRT-PCR. The PCa cells' invasive, migrative, and proliferative activities in vitro were assessed using transwell migration and invasion, wound-healing, cloning creation, and CCK-8 assays. In the present study, impaired proliferative, migrative, and invasive capacities were observed in the NEAT1-deficient PCa (PC3 and LNCaP) cells. Further mechanistic studies found that NEAT1 performs its function through sponging miR-582-5p. Furthermore, EZH2 was confirmed to be the downstream target gene of miRNA-582-5p. The impaired progression caused by NEAT1 deficiency in PCa cells was significantly restored by the inhibition of miR-582-5p, while these effects were largely abolished by the deletion of EZH2. Finally, the xenograft nude mouse model showed that knocking down the expression of NEAT1 suppressed the growth of PCa. In conclusion, NEAT1 promotes the progression of PCa by controlling the miR-582-5p and miR-582-5p-mediated EZH2.

The online version contains supplementary material available at 10.1007/s10616-023-00612-z.

Myocardial infarction (MI) is a cardiovascular disease that seriously threatens human health. However, an immune-related competitive endogenous RNA (ceRNA) network has not been reported in MI.

The GSE66360, GSE19339, GSE97320, GSE61741, and GSE168281 datasets were acquired from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) and differentially expressed miRNAs (DEmiRNAs) from MI patients and healthy controls were screened and an immune-related ceRNA network was constructed. Furthermore, the key long noncoding RNAs(lncRNAs) highly related to the immune mechanism of MI were identified utilizing the random walk with restart algorithm. Finally, the expression of the hub genes was further verified in the GSE66360, GSE19339, and GSE97320 datasets, and quantitativereal-time polymerase chain reaction (qRT-PCR) was performed for the MI patients and healthy controls.

A total of 184 differentially expressed immune-related genes(DE-IRGs) and 432 DE-miRNAs were obtained, and an immune-related ceRNA network comprising 1421 lncRNAs, 61 DE-miRNAs, and 139 DE-IRGs was constructed. According to the order of stress, betweenness, and closeness, NEAT1, KCNQ1OT1, and XIST were identified as key lncRNAs. Moreover, random walk with restart analysis also suggested that NEAT1, KCNQ1OT1, and XIST are key lncRNAs. Subsequently, a ceRNA network of 10 hub genes and 3 lncRNAs was constructed. Finally, we found that the expression of FCER1G and TYROBP significantly differed between MI patients and control individuals in the GSE66360, GSE19339, and GSE97320 datasets. qRT-PCR revealed that the expression of NEAT1, KCNQ1OT1, XIST, FCER1G, and TYROBP was significantly elevated in MI tissue samples compared to healthy control tissue samples.

NEAT1, KCNQ1OT1, XIST, FCER1G, and TYROBP are involved in MI and can be used as molecular biomarkers for the screening and diagnosis of MI. Furthermore, the immune system plays an essential role in the onset and progression of MI.

Prostate cancer, the second most prevalent malignancy among men, poses a significant threat to affected patients' well-being due to its poor prognosis. Novel biomarkers are required to enhance clinical outcomes and tailor personalized treatments. Herein, we describe our research to explore the prognostic value of long non-coding RNAs (lncRNAs) deregulated by copy number variations (CNVs) in prostate cancer.

The study employed an integrative multi-omics data analysis of the prostate cancer transcriptomic, CNV and methylation datasets to identify prognosis-related subtypes. Subtype-specific expression profiles of protein-coding genes (PCGs) and lncRNAs were determined. We analysed CNV patterns of lncRNAs across the genome to identify subtype-specific lncRNAs with CNV changes. LncRNAs exhibiting significant amplification or deletion and a positive correlation were designated CNV-deregulated lncRNAs. A prognostic risk score model was subsequently developed using these CNV-driven lncRNAs.

Six molecular subtypes of prostate cancer were identified, demonstrating significant differences in prognosis (P = 0.034). The CNV profiles of subtype-specific lncRNAs were examined, revealing their correlation with CNV amplification or deletion. Six lncRNAs (CCAT2, LINC01593, LINC00276, GACAT2, LINC00457, LINC01343) were selected based on significant CNV amplifications or deletions using a rigorous univariate Cox proportional risk regression model. A robust risk score model was developed, stratifying patients into high-risk and low-risk categories. Notably, our prognostic model based on these six lncRNAs exhibited exceptional predictive capabilities for recurrence-free survival (RFS) in prostate cancer patients (P = 0.024).

Our study successfully identified a prognostic risk score model comprising six CNV-driven lncRNAs that could potentially be prognostic biomarkers for prostate cancer. These lncRNA signatures are closely associated with RFS, providing promising prospects for improved patient prognostication and personalized therapeutic strategies for novel prostate cancer treatment.

Family selection is an important method in fish aquaculture because growth is the most important economic trait. Fast-and slow-growing families of tiger puffer fish (Takifugu rubripes) have been established through family selection. The development of teleost fish is primarily controlled by the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis that includes the hypothalamus-pituitary-liver. In this study, the molecular mechanisms underlying T. rubripes growth were analyzed by comparing transcriptomes from fast- and slow-growing families. The expressions of 214 lncRNAs were upregulated, and those of 226 were downregulated in the brain tissues of the fast-growing T. rubripes family compared to those of the slow-growing family. Differentially expressed lncRNAs centrally regulate mitogen-activated protein kinase (MAPK) and forkhead box O (FoxO) signaling pathways. Based on the results of lncRNA-gene network construction, we found that lncRNA3133.13, lncRNA23169.1, lncRNA23145.1, and lncRNA23141.3 regulated all four genes (igf1, mdm2, flt3, and cwf19l1). In addition, lncRNA7184.10 may be a negative regulator of rasgrp2 and a positive regulator of gadd45ga, foxo3b, and dusp5. These target genes are associated with the growth and development of organisms through the PI3K/AKT and MAPK/ERK pathways. Overall, transcriptomic analyses of fast- and slow-growing families of T. rubripes provided insights into the molecular mechanisms of teleost fish growth rates. Further, these analyses provide evidence for key genes related to growth regulation and the lncRNA expression regulatory network that will provide a framework for improving puffer fish germplasm resources.

Vernalization plays a crucial role in the flowering and yield of Chinese cabbage, a process intricately influenced by long non-coding RNAs (lncRNAs). Our research focused on lncFLC1, lncFLC2a, and lncFLC2b, which emerged as key players in this process. These lncRNAs exhibited an inverse expression pattern to the flowering repressor genes FLOWERING LOCUS C 1 (BrFLC1) and FLOWERING LOCUS C 2 (BrFLC2) during vernalization, suggesting a complex regulatory mechanism. Notably, their expression in the shoot apex and leaves was confirmed through in fluorescent in situ hybridization (FISH). Furthermore, when these lncRNAs were overexpressed in Arabidopsis, a noticeable acceleration in flowering was observed, unveiling functional similarities to Arabidopsis's COLD ASSISTED INTRONIC NONCODING RNA (COOLAIR). This resemblance suggests a potentially conserved regulatory mechanism across species. This study not only enhances our understanding of lncRNAs in flowering regulation, but also opens up new possibilities for their application in agricultural practices.

We evaluated the involvement of lncRNAs in the development of pathologies associated with chronic hyperglycaemia in rat models in a model of type 1, type 2 and gestational diabetes.

Reports were searched in Dialnet, Scielo, HINARI, Springer, ClinicalKey, OTseeker, PubMed and different grey literature databases with any restrictions. Bibliography databases will be searched from their inception to December 2022.

Thirty-seven studies met our criteria, and they had the following characteristics: original experimental studies on diabetes, the lncRNAs were extracted or measured from tissues of specific areas and the results were expressed in terms of standard measures by RT-PCR. In most studies, both primary and secondary outcomes were mentioned. On the other hand, we found a total of nine diabetic complications, being retinopathy, nephropathy and neuropathy the most representatives. Additionally, it was found that MALAT1, H19, NEAT1 and TUG1 are the most studied lncRNAs about these complications in rats. On the other hand, the lncRNAs with the highest rate of change were MSTRG.1662 (17.85; 13.78, 21.93), ENSRNOT00000093120_Aox3 (7.13; 5.95, 8.31) and NONRATG013497.2 (-5.55; -7.18, -3.93).

This review found a significant involvement of lncRNAs in the progression of pathologies associated with chronic hyperglycaemia in rat models, and further studies are needed to establish their potential as biomarkers and therapeutic targets for diabetes.

Dysregulation of the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been linked to some oncogenic pathways that induce cancer initiation and progression. This meta-analysis was conducted to specifically summarize the most recent research on MALAT1 function in human gastric cancer (GC).

The eligible studies were first identified by searching HowNet, Web of Science, PubMed, The Cochrane Library, Embase, and Nature databases for studies published as of April 1, 2023. The meta-analysis included 14 studies assessing MALAT1 expression and presenting clinical parameters and survival outcomes.

The results illustrated that high MALAT1 expression is predictive of lymph node metastasis (pooled odds ratio [OR] = 2.99, 95% confidence interval [CI] = 1.97-4.54, P < 0.001) and distant metastasis in GC (OR = 3.11, 95% CI = 1.68-5.75, P < 0.001). In addition, MALAT1 was associated with GC tumor invasion (T3/T4 vs. T1/T2: OR = 2.90, 95% CI = 1.90- 4.41, P <0.001) and TNM stage (III/IV vs I/II: OR = 2.93, 95% CI: 1.80-4.77, P <0.001). Additionally, higher MALAT-1 expression predicted poorer overall survival in patients with GC (hazard ratio = 1.64, 95% CI = 1.20-2.09, P < 0.001).

The current findings suggest that the high MALAT1 expression is an adverse biomarker for prognostic outcomes, lymph node metastasis, TNM stage, and distant metastasis in GC and MALAT1 could be a prognostic biomarker for GC.

Renal interstitial fibrosis (RIF) represents an irreversible and progressive pathological manifestation of chronic renal disease, which ultimately leads to end-stage renal disease. Long noncoding RNAs (lncRNAs) have been suggested to be involved in the progression of RIF. Small nucleolar RNA host gene 16 (SNHG16), a member of lncRNAs, has been found to be involved in the progression of pulmonary fibrosis. This paper first researched the effect of SNHG16 on renal fibrosis. We established a unilateral ureteral obstruction (UUO)-induced mouse RIF model by ligation of the left ureter to evaluate the biological function of SNHG16 in RIF. As a result, SNHG16 was upregulated in UUO-induced renal fibrotic tissues. Knockdown of SNHG16 inhibited RIF and reduced alpha-smooth muscle actin (α-SMA), fibronectin, and college IV expression. miR-205 was a target of SNHG16, and downregulated in UUO-induced renal fibrotic tissues. Inhibition of miR-205 promoted RIF and increased the expression of α-SMA, college IV, and fibronectin. Overexpression of SNHG16 promoted the UUO-induced RIF, but miR-205 abrogated this effect of SNHG16. Histone deacetylase 5 (HDAC5) showed high expression in UUO-induced renal fibrotic tissues. Knockdown of HDAC5 significantly reduced α-SMA, fibronectin, and college IV expression in renal tissues of UUO-induced mice. Inhibition of miR-205 promoted HDAC5 expression, but knockdown of SNHG16 inhibited HDAC5 expression in renal tissues of UUO-induced mice. In conclusion, SHNG16 is highly expressed in renal fibrotic tissues of UUO-induced mice. Knockdown of SHNG16 may prevent UUO-induced RIF by indirectly upregulating HDAC5 via targeting miR-205. SHNG16 may be novel target for treating renal fibrosis.

Long non-coding RNAs (lncRNAs) have been discovered through many studies to play a crucial role in tumor progression. LncRNA PCAT5 has been identified as a human cancer-related gene in diverse cancers. However, the specific role of PCAT5 in esophageal squamous cell carcinoma (ESCC) still needs further study. The study aimed to test the PCAT5 expression and find its biological function in ESCC. Functional experiments, including EdU, transwell and TUNEL, were done in the chosen ESCC cell lines under silenced PCAT5. Luciferase reporter and Western blot experiments were implemented to ensure the possible regulatory mechanism involved in ESCC. PCAT5 presented higher expression in ESCC cells in comparison to normal cells. The silence of PCAT5 restrained ESCC cell abilities of proliferation, migration and invasion. On the contrary, it accelerated ESCC cell apoptosis. The results of rescue experiments showed that PCAT5 regulated ESCC cell proliferative, migrated, invasive and apoptotic abilities via sponging miR-4295 to up-regulate PHF20.

The natural phenolic compound ellagic acid exerts anti-cancer effects, including activity against colorectal cancer (CRC). Previously, we reported that ellagic acid can inhibit the proliferation of CRC, and can induce cell cycle arrest and apoptosis. This study investigated ellagic acid-mediated anticancer effects using the human colon cancer HCT-116 cell line. After 72 h of ellagic acid treatment, a total of 206 long noncoding RNAs (lncRNAs) with differential expression greater than 1.5-fold were identified (115 down-regulated and 91 up-regulated). Furthermore, the co-expression network analysis of differentially expressed lncRNA and mRNA showed that differential expressed lncRNA might be the target of ellagic acid activity in inhibiting CRC.

Lung adenocarcinoma (LUAD) is one of the most common and lethal cancer types worldwide. LINC0572 is a long non-coding RNA (lncRNA) that has been associated with the clinical characteristics of several types of malignancy. However, the biological mechanism of LINC0572 in LUAD is still unclear and remains to be elucidated.

R packages and online bioinformatic tools were used to investigate the biological characteristics of LINC01572, including its abnormal expression, oncogenic role, and clinical prognostic value. In vitro and in vivo experiments were conducted to investigate the biological functions of LINC01572 in tumorigenesis and development. These included colony formation assays, cell migration assays, flow cytometry, cell counting kit-8 (CCK-8) cell proliferation and tumor transplant growth experiments.

Bioinformatics results showed that LINC01572 was overexpressed in both LUAD and lung squamous cell carcinoma (LUSC) patients. LINC01572 overexpression was associated with shorter overall survival (OS) in LUAD. Further study of clinical specimens confirmed that LINC01572 was highly expressed in the tumor tissue of non-small cell lung cancer (NSCLC) patients. In vitro experiments also confirmed that LINC01572 was overexpressed in tumor cell lines. Inhibition of LINC01572 expression significantly impaired cell proliferation, cell migration, and clone formation. Experiments in nude mouse revealed that transplanted tumors with low expression of LINC01572 had significantly slower rates of growth in terms of volume and weight compared to the control group (p < 0.05). In addition, gene set enrichment analysis (GSEA) and immune landscape profiling showed that LINC01572 can promote tumor initiation and progression by deregulating the cell cycle and immunocyte infiltration.

LINC01572 is overexpressed in tumor tissue relative to adjacent normal tissue. Moreover, LUAD patients with high expression of LINC01572 showed a worse survival prognosis. LINC01572 is associated with tumor initiation, progression and immune dysregulation. It therefore has potential value as a novel biomarker and therapeutic target in LUAD.

Folic acid is a water-soluble B vitamin (B9), which is closely related to the body's immune and other metabolic pathways. The folic acid synthesized by rumen microbes has been unable to meet the needs of high-yielding dairy cows. The incidence rate of subclinical mastitis in dairy herds worldwide ranged between 25%~65% with no obvious symptoms, but it significantly causes a decrease in lactation and milk quality. Therefore, this study aims at exploring the effects of folic acid supplementation on the expression profile of lncRNAs, exploring the molecular mechanism by which lncRNAs regulate immunity in subclinical mastitic dairy cows.

The analysis identified a total of 4384 lncRNA transcripts. Subsequently, differentially expressed lncRNAs in the comparison of two groups (SF vs. SC, HF vs. HC) were identified to be 84 and 55 respectively. Furthermore, the weighted gene co-expression network analysis (WGCNA) and the KEGG enrichment analysis result showed that folic acid supplementation affects inflammation and immune response-related pathways. The two groups have few pathways in common. One important lncRNA MSTRG.11108.1 and its target genes (ICAM1, CCL3, CCL4, etc.) were involved in immune-related pathways. Finally, through integrated analysis of lncRNAs with GWAS data and animal QTL database, we found that differential lncRNA and its target genes could be significantly enriched in SNPs and QTLs related to somatic cell count (SCC) and mastitis, such as MSTRG.11108.1 and its target gene ICAM1, CXCL3, GRO1.

For subclinical mastitic cows, folic acid supplementation can significantly affect the expression of immune-related pathway genes such as ICAM1 by regulating lncRNAs MSTRG.11108.1, thereby affecting related immune phenotypes. Our findings laid a ground foundation for theoretical and practical application for feeding folic acid supplementation in subclinical mastitic cows.

The tumor microenvironment (TME) is an intricate ecosystem that is actively involved in various stages of cancer occurrence and development. Some characteristics of tumor biological behavior, such as proliferation, migration, invasion, inhibition of apoptosis, immune escape, angiogenesis, and metabolic reprogramming, are affected by TME. Studies have shown that non-coding RNAs, especially long-chain non-coding RNAs and microRNAs in cancer-derived exosomes, facilitate intercellular communication as a mechanism for regulating angiogenesis. They stimulate tumor growth, as well as angiogenesis, metastasis, and reprogramming of the TME. Exploring the relationship between exogenous non-coding RNAs and tumor-associated endothelial cells, as well as their role in angiogenesis, clinicians will gain new insights into treatment as a result.

Long non-coding RNA (lncRNA) PTCSC3 is characterized as a tumor suppressor in thyroid cancer and glioma. The present study aimed to investigate the role of PTCSC3 in triple-negative breast cancer (TNBC). A total of 82 patients with TNBC were enrolled in the present study. The results showed that PTCSC3 was downregulated, while lncRNA MIR100HG was upregulated in tumor tissues compared with that in adjacent non-cancerous tissues of patients with TNBC. The follow-up study showed that low expression levels of PTCSC3 and high expression levels of MIR100HG were closely associated with poor survival of patients with TNBC. The expression levels of MIR100HG were decreased with the clinic stages of TNBC, while the expression levels of MIR100HG showed the opposite trend. Correlation analysis showed that the expression levels of PTCSC3 and MIR100HG were significantly correlated in both tumor tissues and adjacent non-cancerous tissues. The overexpression of PTCSC3 inhibited the expression level of MIR100HG in TNBC cells, while the expression level of PTCSC3 was unaffected. Cell Counting Kit-8 and Annexin V-FITC Apoptosis flow cytometry assays showed that overexpression of PTCSC3 led to inhibition, while overexpression of MIR100HG led to the promotion of TNBC cells viability and inhibited apoptosis of TNBC cells. In addition, overexpression of MIR100HG attenuated the effects of PTCSC3 overexpression on cancer cell viability. However, the overexpression of PTCSC3 did not affect cancer cell migration and invasion. Western-blot analysis showed that PTCSC3 suppressed viability and promoted apoptosis of TNBC cells through the Hippo signaling pathway. Thus, the present study demonstrated that lncRNA PTCSC3 inhibits cancer cell viability and promotes cancer cell apoptosis in TNBC by downregulating MIR100HG.

Nowadays, primary liver cancer is still a major threat to human health. Anoikis is a particular form of programed cell death that has an inhibitory effect on neoplasm metastasis. Although several prognostic models based on anoikis-related genes for Hepatocellular carcinoma (HCC) have been established, signatures associated with anoikis-related lncRNAs have not been identified. To fill this blank space, the authors built up a prognostic signature and appraised its value in guiding immunotherapy. Eleven prognostic anoikis-related lncRNAs were identified through Least Absolute Shrinkage and Selection Operator Cox analysis. The accuracy of the risk signature in predicting prognosis was verified by K-M survival analysis and Receiver operating characteristic analysis. We further discovered that the high-risk group was often enriched in signal pathways related to cell growth and death and immune response; in addition, in the low-risk group, cells often undergo metabolic changes through gene set enrichment analysis. Finally, we realised that HCC patients in the high-risk group were upregulated in immune-checkpoint molecules and tend to have a higher tumour mutation burden level which indicated a higher sensitivity to immunotherapy. All in all, the anoikis-related lncRNAs risk signature showed excellent ability in predicting prognosis and may guide the application of immunotherapy in future clinical practice.

Long non-coding RNAs (lncRNAs) are master regulators of gene expression and have recently emerged as potential innovative therapeutic targets. The deregulation of lncRNA expression patterns has been associated with age-related and noncommunicable diseases in the bone tissue, including osteoporosis and tumors. However, the specific role of lncRNAs in physiological or pathological conditions in the bone tissue still needs to be further clarified, for their exploitation as therapeutic tools. In the present study, we evaluate the potential of the lncRNA CASC2 as a regulator of osteogenic differentiation and mineralization. Results show that CASC2 expression is decreased during osteogenic differentiation of human bone marrow-derived Mesenchymal Stem/Stromal cells (hMSCs). CASC2 knockdown, using small interfering RNA against CASC2 (siCASC2), increases the expression of the late osteogenic marker Bone Sialoprotein (BSP), but does not impact ALP staining level nor the expression of early osteogenic transcripts, including RUNX2 and OPG. Although siCASC2 does not impact hMSC proliferation nor apoptosis, it promotes the mineralization of hMSC cultured under osteogenic-inducing conditions, as shown by the increase of calcium deposits. Mass spectrometry-based proteomic analysis revealed that 89 proteins are regulated by CASC2 at late osteogenic stages, including proteins associated with bone diseases or anthropometric and musculoskeletal traits. Specifically, the Cartilage Oligomeric Matrix Protein (COMP) is highly enhanced by CASC2 knockdown at late stages of osteogenic differentiation, at both transcriptional and protein level. On the other hand, inhibition of COMP impairs osteoblasts mineralization as well as the expression of BSP. The results indicate that lncRNA CASC2 regulates late osteogenic differentiation and mineralization in hMSC via COMP and BSP. In conclusion, this study suggests that targeting lncRNA CASC2 could be a potential approach for modulating bone mineralization.

Noncoding RNAs (ncRNAs), which make up a significant portion of the mammalian transcriptome and plays crucial regulatory roles in expression of genes and other biological processes, have recently been found. The most extensively researched of the sncRNAs, microRNAs (miRNAs), have been characterized in terms of their synthesis, roles, and significance in the tumor development. Its crucial function in the stem cell regulation, another class of sncRNAs known as aspirRNAs, has attracted attention in cancer research. The investigations have shown that long non-coding RNAs have a crucial role in controlling developmental stages, such as mammary gland development. Additionally, it has been discovered that lncRNA dysregulation precedes the development of several malignancies, including breast cancer. The functions of sncRNAs (including miRNAs and piRNAs) and lncRNAs in the onset and development of the breast cancer are described in this study. Additionally, future perspectives of various ncRNA-based diagnostic, prognostic, and therapeutic approaches also discussed.

Long noncoding RNA ubiquitin-conjugating enzyme E2 R2 antisense RNA 1 (UBE2R2-AS1) has been recently reported to participate in the progression of tumors, including glioma and liver cancer. However, the roles of UBE2R2-AS1 in prostate cancer (PC) remained poorly understood.

The expression of UBE2R2-AS1 was determined in tumor tissues and paired adjacent tissues from PC patients using quantitative reverse transcription PCR analysis. Correlation between UBE2R2-AS1 expression and clinicopathological parameters and overall survival were investigated by Chi-square test and Kaplan-Meier method analysis. The in vitro experiments, including CCK-8 assay, colony formation, flow cytometry and transwell assay were performed to investigate the functional role of UBE2R2-AS1 knockdown or overexpression on PC cell lines (PC-3 and DU145). Related protein expression levels were measured by western blot analysis.

Our data showed that UBE2R2-AS1 expression was significantly upregulated in PC tissues compared with that in adjacent tissues. The high levels of UBE2R2-AS1 were associated with high Gleason score, advanced clinical T stage, lymph node metastasis and poor prognosis. Knockdown of UBE2R2-AS1 suppressed cell proliferation, migration and invasion, induced cell cycle G0/G1 arrest and apoptosis in PC cells, along with decreased expression of PCNA, CDK4, Cyclin D1, Bcl-2, N-cadherin and Vimentin, and increased E-cadherin expression. Overexpression of UBE12R2-AS1 obtained the opposite results in PC cells.

Our findings suggest that UBE2R2-AS1 might be a potential diagnostic and/or therapeutic target in PC.

Melanoma is the most lethal skin cancer with increasing incidence worldwide. Despite a great improvement of diagnostics and treatment of melanoma patients, this disease is still a serious clinical problem. Therefore, novel druggable targets are in focus of research. EZH2 is a component of the PRC2 protein complex that mediates epigenetic silencing of target genes. Several mutations activating EZH2 have been identified in melanoma, which contributes to aberrant gene silencing during tumor progression. Emerging evidence indicates that long non-coding RNAs (lncRNAs) are molecular "address codes" for EZH2 silencing specificity, and targeting lncRNAs-EZH2 interaction may slow down the progression of many solid cancers, including melanoma. This review summarizes current knowledge regarding the involvement of lncRNAs in EZH2-mediated gene silencing in melanoma. The possibility of blocking lncRNAs-EZH2 interaction in melanoma as a novel therapeutic option and plausible controversies and drawbacks of this approach are also briefly discussed.