Cancer has high mortality rate and occupies second position among major diseases. Despite extensive research and therapies, in every nook and corner of the world, death rate is increasing exponentially. Hallmarks of cancer are benchmarks of cancer cells describing the fundamental principle and capabilities of the cells transforming from normal to malignant tumour. One of the major ones among them is the deregulation of cellular metabolism or metabolic reprogramming, involving alterations in glucose and lipid metabolism. Progressive research in this area has visualized the vital role of lncRNAs in lipid metabolism with respect to AML. lncRNAs involve in various cellular processes and also contribute for significant functions of the cell like chromatin remodelling, transcriptional activation and repression, gene regulation, immune response, cell differentiation, and cell cycle regulation, in addition to oncogenic processes such as proliferation, angiogenesis, migration, and apoptosis. Structural similarities are observed among mRNAs and lncRNAs in terms of poly A-tail and 5' cap however protein-coding regions are lacking. A large body of evidence has shown that lncRNAs directly or indirectly mediate lipid metabolism by activating downstream genes. Considering their potential involvement in leukemia, these lncRNAs can be explored and considered as biomarkers for therapeutics, prognosis, and diagnosis. The present review is planned to summarize the functional classification of lncRNAs, the role of lipid metabolism in cancer, different lncRNAs involved in leukemia, and different cancer types related to lipid metabolism.

Long non-coding RNAs (lncRNAs) have emerged as critical regulators in cancer biology, influencing tumor initiation, progression, and metastasis. Among them, GAPLINC (Gastric Adenocarcinoma Predictive Long Intergenic Non-coding RNA) has garnered attention due to its aberrant expression across various malignancies and its association with poor clinical outcomes. While several studies have highlighted GAPLINC's oncogenic roles through interactions with microRNAs and involvement in epithelial-mesenchymal transition (EMT), a comprehensive synthesis of its mechanistic functions and clinical implications remains limited. This review addresses this limitation by systematically analyzing current findings on GAPLINC's molecular mechanisms, regulatory networks, and functional roles in different cancer types, including gastric, colorectal, non-small cell lung cancer (NSCLC), glioma, renal cell carcinoma (RCC), and esophageal squamous cell carcinoma (ESCC). We further evaluate the potential of GAPLINC as a diagnostic, prognostic, and therapeutic target, providing an integrated perspective that consolidates existing knowledge and identifies directions for future research. By highlighting both common and cancer-specific mechanisms involving GAPLINC, this review adds new insights into its significance as a versatile biomarker and therapeutic target in oncology.

Animal and plant male sterility is a complex and closely studied phenomenon that significantly impacts species survival and reproduction. Advances in biotechnology and molecular biology have deepened our understanding of gene expression regulation, particularly the role of noncoding RNAs (ncRNAs). This study aims to systematically review and analyze the published literature on ncRNAs in relation to both animal and plant sterility using bibliometric methods. A bibliometric analysis was conducted with CiteSpace 6.2.R6, Scimago Graphica, VOSviewer 1.6.18, and Microsoft Excel 2016 to identify research hotspots, key developments, and emerging trends. Data were retrieved from the Web of Science Core Collection on March 3, 2024, covering publications from 2005 to 2023. The analysis revealed a consistent increase in annual publications on ncRNA research in both plant and animal fields, with China and the United States leading in publication volume. Notable scholars include Professor Abu-Halima, a prominent figure in ncRNA research related to animal male sterility, and Professor Meyers, a key contributor to plant male sterility research. Journals such as PLoS ONE serve as major platforms for disseminating findings on animal male sterility, while The Plant Cell plays a similar role for plant male sterility. Analysis of cited literature and keyword trends highlighted significant themes, including gene regulation and the application of novel technologies. At present, new technologies, model organisms, and gene regulation remain major research hotspots. Meanwhile, disease diagnosis, disease treatment, and crop improvement are emerging as important directions for future research.

Polyploid giant cancer cells (PGCCs) are characterized by enlarged nuclei, association with tumors, and resistance to treatment, contributing significantly to cellular heterogeneity. These cells arise from endoreplication and cell fusion, often triggered by stressors such as radiation and chemotherapy. PGCCs exhibit chromosomal instability and aneuploidy, leading to poor prognosis in various cancers. Key features include the ability to produce progeny cells via amitotic division and the expression of cancer stem cell markers. PGCC formation and function involve signaling pathways like cell fusion (GCM1/syncytin-1), cell cycle control, stress response, and EMT. Understanding these pathways is crucial for identifying therapeutic targets. Current therapeutic strategies targeting PGCCs involve drugs like azacitidine, decitabine, and zoledronic acid, as well as DNMT inhibitors in combination therapies. These approaches aim to reverse drug resistance and enhance antitumor efficacy. Furthermore, microRNAs (miRNAs) are pivotal in regulating gene expression and influencing the cell cycle, proliferation, and apoptosis. Cataloging miRNAs and understanding their function is critical for developing potential cancer treatments. Researchers are exploring miRNA-based modulation of signaling pathways to block tumor growth. This review highlights the complex biology of PGCCs and emphasizes the need for targeted therapies to improve cancer treatment outcomes.

Thyroid cancer (TC) represents the most common endocrine malignancy; however, the intricacies of its carcinogenesis pose significant challenges to therapeutic interventions. A comprehensive understanding of the molecular mechanisms that drive TC progression is crucial for the development of effective treatment strategies, especially considering the increasingly recognized role of non-coding RNAs (ncRNAs) in oncogenesis. Notwithstanding recent advancements, the regulatory functions of long non-coding RNAs (lncRNAs) and their interactions with microRNAs (miRNAs) in the context of TC are not yet fully elucidated. This review aims to address this knowledge deficiency by investigating the dual roles of lncRNAs in the pathogenesis of TC, specifically their regulation of programmed cell death (PCD) pathways. Current literature indicates that disrupted competitive endogenous RNA (ceRNA) networks are involved in drug resistance, epithelial-mesenchymal transition (EMT), as well as tumor proliferation, angiogenesis, invasion, and metastasis in TC. The basis of cancer therapy-induced tumor cell elimination is programmed cell death (PCD), which includes well-studied processes such as apoptosis, autophagy, and ferroptosis as well as novel pathways, such as cuproptosis, immunogenic cell death (ICD), and PANoptosis. Recent research has shown the critical function of long non-coding RNAs (lncRNAs) in modifying these several PCD pathways, impacting TC growth and therapy response. This review synthesizes evidence on how lncRNAs regulate PCD to influence TC progression and therapeutic outcomes. Additionally, we examine the clinical relevance of lncRNAs in TC, highlighting their potential as biomarkers for diagnosis and prognosis, therapeutic targets, and contributors to drug resistance, while emphasizing recent advancements in this field.

Gut microbiome has a considerable impact on the central nervous system via the "gut-brain axis." Neuroepigenome emerges as the interface between environment and genes, potentially help conveying the signals derived from the microbiome to the brain tissue. While only a limited number of studies have implicated epigenetic roles in the gut-brain axis, this review explores how gut microbiome might impact various brain-based epigenetic mechanisms, including DNA methylation, histone modification, ncRNA and RNA methylation, notably in the context of the specific neural complications. Among the epigenetic mechanisms, histone acetylation was most well-studied with respect to its relationships with gut microbiome, exerting a dynamic influence on gene expression in the brain. Furthermore, the pathways connecting gut bacteria to neuroepigenome were summarized, highlighting the roles of metabolites such as butyrate, propionate, acetate, lactate, and folate. Of particular interest, the roles of butyrate are emphasized due to their outstanding inhibitory activity towards histone deacetylases (HDACs), among other mechanisms. It is worth noting that some indirect gut-brain pathways may also be associated with the interplay between microbiome and neuroepigenome, while IL-6 has been found to effectively transmit microbe-derived signals to histone methylation in brains. Finally, we recapitulate the future perspectives critical to understanding this gut-brain crosstalk, such as clarifying the cause-and-effect relationship, bacterial cross-feeding within the gut, and the mechanisms underlying the site-specific histone modification in the brain. Together, this review attempts to consolidate our current knowledge about the "microbiome-neuroepigenome interplay" and propose a conceptual pathway to decipher the gut-brain axis in various neurological conditions.

Cervical cancer (CC) is the primary cause of cancer-related mortality among women in developing countries and is the most prevalent disease linked to human papillomavirus (HPV). Over 70 % of CC cases result from persistent infections with high-risk HPV types. The virus typically targets the mucocutaneous epithelium, generating viral particles in mature epithelial cells, which leads to disruptions in normal cell-cycle regulation and promotes uncontrolled cellular proliferation. This unchecked cell division results in the accumulation of genetic damage, contributing to the pathogenesis of CC. While HPV infection is a key etiological factor, the disease's progression also necessitates the involvement of genetic and epigenetic influences. One of the epigenetic regulators, long noncoding RNAs (lncRNAs), are characterized by transcripts exceeding 200 nucleotides. These molecules play crucial roles in various cellular processes, including transcription regulation, RNA metaboli35 per 100,000sm, and apoptosis. Investigating the specific roles of lncRNAs in modulating gene expression related to the oncogenic mechanisms of CC, particularly in the context of high-risk HPV infections, may provide valuable insights for diagnostic and therapeutic advancements. Herein, we first review key molecular mechanisms by which lncRNAs interfere with CC-related HPV development. Then, diagnostic, prognostic, and therapeutic potentials of these lncRNA molecules will be highlighted in depth. The focus of this article is on the role of lncRNAs associated with HPV-related CC, emphasizing the investigation of signaling pathways and their underlying molecular mechanisms. Furthermore, we explore the therapeutic potential and diagnostic relevance of the most significant lncRNAs in the context of CC, thereby highlighting their importance in advancing treatment strategies and improving patient outcomes.

Egg production performance a critical economic trait in the poultry industry. The regulatory mechanisms underlying egg production performance mediated by non-coding RNAs remain to be characterized. To systematically investigate ovarian lncRNAs, circRNAs, and miRNAs associated with laying efficiency, we conducted comparative transcriptomic analyses using RNA sequencing (RNA-seq) of ovarian tissues from phenotypically divergent groups - high egg production (HEP) and low egg production (LEP) hens. In our study, we identified 675 lncRNAs, 140 circRNAs, and 10 miRNAs that were significantly differentially expressed (DE) between HEP and LEP. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that target genes of DE lncRNAs, DE miRNAs, and the source genes of DE circRNAs are involved in the MAPK signaling pathway, endocytosis, notch signaling pathway, among others. Furthermore, we identified five miRNA-mRNA interactions related to egg production including gga-miR-449c-3p, and five genes (GLI2, TAC1, EML6, THOC3, MMP9). These findings establish the first comprehensive ncRNA interactome driving ovarian efficiency, offering both biomarkers for breeding selection and mechanistic targets for reproductive enhancement.

Genome sequencing has enabled us to find functional peptides encoded by short open read frames (sORFs) in long non-coding RNAs (lncRNAs). sORFs-encoded peptides (SEPs) regulate gene expression, signaling, and so on and have significant roles, unlike common peptides. Various computational methods have been proposed. However, there is a lack of contributive features and effective models. Therefore, a high-throughput computational method to predict SEPs is needed.

We propose a computational method, SORFPP, to predict SEPs by mining feature information from multiple perspectives in an experimentally validated dataset from TranLnc. SORFPP fully extracts SEP sequence information using the protein language model ESM-2 and curated traditional encoding, including QSOrder, k-mer, etc. SORFPP uses CatBoost to solve the sparsity problem of traditional encoding. SORFPP also analyzes ESM-2 pre-training characterization information with the Self-attention model. Finally, an ensemble learning framework combines the two models and their results are fed into Logistic Regression model for accurate and robust predictions. For comparison, SORFPP outperforms other state-of-the-art models in Matthew correlation coefficient by 12.2%-24.2% on three benchmark datasets.

Integrating the ensemble learning strategy with contributive traditional features and the protein language encoding methods shows better performance. Datasets and codes are accessible at https://doi.org/10.6084/m9.figshare.28079897 and http://111.229.198.94:5000/.

Deep learning holds great promise in drug discovery, yet its application is hindered by high labeling costs and limited datasets. Developing algorithms that effectively learn from sparsely labeled data is crucial. Capsule networks (CapsNet), introduced in 2017, solve the spatial information loss in traditional neural networks and excel in handling small datasets by capturing spatial hierarchical relationships among features. This capability makes CapsNet particularly promising for drug discovery, where data scarcity is a common challenge. Various modified CapsNet architectures have been successfully applied to drug design and discovery tasks. This review provides a comprehensive analysis of CapsNet's theoretical foundations, its current applications in drug discovery, and its performance in addressing key challenges in the field. Additionally, the study highlights the limitations of CapsNet and outlines potential future research directions to further enhance its utility in drug discovery, offering valuable insights for researchers in both computational and pharmaceutical sciences.

Weightless bone loss is a common pathological phenomenon in weightless environments, yet its specific molecular mechanism remain incompletely elucidated. The aim of this study was to systematically investigate the differential expression profiles of mRNAs and long noncoding RNAs (lncRNAs) to explore the molecular pathogenesis underlying weightless bone loss.

Transcriptome sequencing was performed on bone marrow mesenchymal stem cell (BMSCs) samples from the Ground control group and simulated microgravity (SMG) group using Illumina technology. Using the DESeq2 algorithm, we accurately identify and analyzed the differentially expressed genes (DEGs). Subsequently, the molecular functions and signaling pathways enriched by DEG were comprehensively analyzed by GO and KEGG. In addition, by constructing lncRNA-mRNA coexpression network, this study screened and verified key lncRNAs as potential genes to further explore their role in the occurrence and development of weightless bone loss.

A total of 215 differentially expressed lncRNAs (DElncRNAs) and 381 differentially expressed mRNAs (DEmRNAs) were identified, in the SMG group. DEmRNAs were primarily involved in the cell response to mechanical stimulation, microtubule motility and TNF signaling pathway. Meanwhile, DElncRNAs are significantly enriched in cell differentiation, fatty acid metabolic process and biosynthesis of amino acids. In addition, the expression levels of related lncRNAs and mRNAs in weightless bone loss were verified via qRT-PCR. lncRNA-mRNA coexpression network found that lncRNA Ubr5 closely related to osteoblast proliferation and differentiation. Further experimental results revealed that knocking down lncRNA Ubr5 can promote the apoptosis of BMSCs and inhibit their proliferation and osteogenic differentiation.

This study revealed the molecular pathogenesis of weightless bone loss, identified lncRNA Ubr5 as a potential intervention target, and provided an important scientific basis and strategic guidance for the prevention and treatment of weightless bone loss.

Cancer is a rising issue worldwide, and numerous studies have focused on understanding the underlying reasons for its occurrence and finding proper ways to defeat it. By applying technological advances, researchers are continuously uncovering and updating treatments in cancer therapy. Their vast functions in the regulation of cell growth and proliferation and their significant role in the progression of diseases, including cancer. This review provides a comprehensive analysis of ncRNAs in breast cancer, focusing on long non-coding RNAs such as HOTAIR, MALAT1, and NEAT1, as well as microRNAs such as miR-21, miR-221/222, and miR-155. These ncRNAs are pivotal in regulating cell proliferation, metastasis, drug resistance, and apoptosis. Additionally, we discuss experimental approaches that are useful for studying them and highlight the advantages and challenges of each method. We then explain the results of these clinical trials and offer insights for future studies by discussing major existing gaps. On the basis of an extensive number of studies, this review provides valuable insights into the potential of ncRNAs in cancer therapy. Key findings show that even though the functions of ncRNAs are vast and undeniable in cancer, there are still complications associated with their therapeutic use. Moreover, there is an absence of sufficient experiments regarding their application in mouse models, which is an area to work on. By emphasizing the crucial role of ncRNAs, this review underscores the need for innovative approaches and further studies to explore their potential in cancer therapy.

Autoimmune diseases (ADs) are a group of complex, chronic conditions characterized by disturbance of immune tolerance, with examples including systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, and psoriasis. These diseases have unclear pathogenesis, and traditional therapeutic approaches remain limited. However, advances in high-throughput histology technology and scientific discoveries have led to the identification of various pathogenic factors contributing to ADs. Coupled with improvements in RNA nucleic acid-based drug synthesis, design, and delivery, RNA-based therapies have been extensively investigated for their potential in treating ADs. This paper reviews the progress in the use of miRNAs, lncRNAs, circRNAs, siRNAs, antisense oligonucleotides (ASOs), aptamers, mRNAs, and other RNA-based therapies in ADs, focusing on their therapeutic potential and application prospects, providing insights for future research and clinical treatment of autoimmune diseases.

Bone is a highly calcified and vascularized tissue. The vascular system plays a vital role in supporting bone growth and repair, such as the provision of nutrients, growth factors, and metabolic waste transfer. Moreover, the additional functions of the bone vasculature, such as the secretion of various factors and the regulation of bone-related signaling pathways, are essential for maintaining bone health. In the bone microenvironment, bone tissue cells play a critical role in regulating angiogenesis, including osteoblasts, bone marrow mesenchymal stem cells (BMSCs), and osteoclasts. Osteogenesis and bone angiogenesis are closely linked. The decrease in osteogenesis and bone angiogenesis caused by aging leads to osteoporosis. Long noncoding RNAs (lncRNAs) are involved in various physiological processes, including osteogenesis and angiogenesis. Recent studies have shown that lncRNAs could mediate the crosstalk between angiogenesis and osteogenesis. However, the mechanism by which lncRNAs regulate angiogenesis‒osteogenesis crosstalk remains unclear. In this review, we describe in detail the ways in which lncRNAs regulate the crosstalk between osteogenesis and angiogenesis to promote bone health, aiming to provide new directions for the study of the mechanism by which lncRNAs regulate bone metabolism.

Human cells generate a vast complexity of noncoding RNAs, the "RNA dark matter," which includes a vast small RNA (sRNA) transcriptome. The biogenesis, biological relevance, and mechanisms of action of most of these transcripts remain unknown, and they are widely assumed to represent degradation products. Here, we aimed to functionally characterize human sRNA transcriptome by attempting to answer the following question-can a significant number of novel sRNAs correspond to novel members of known classes, specifically, microRNAs (miRNAs)? By developing and validating a miRNA discovery pipeline, we show that at least 2726 novel canonical miRNAs, majority of which represent novel miRNA families, exist in just one human cell line compared to just 1914 known miRNA loci. Moreover, potentially tens of thousands of miRNAs remain to be discovered. Strikingly, many novel miRNAs map to exons of protein-coding genes emphasizing a complex and interleaved architecture of the genome. The existence of so many novel members of a functional class of sRNAs suggest that the human sRNA transcriptome harbors a multitude of novel regulatory molecules. Overall, these results suggest that we are at the very beginning of understanding the true functional complexity of the sRNA component of the "RNA dark matter."

p16INK4a is a crucial tumor suppressor and regulator of cellular senescence, forming a molecular bridge between aging and cancer. Dysregulated p16INK4a expression is linked to both premature aging and cancer progression, where non-coding RNAs (ncRNAs) such as long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and small interfering RNAs (siRNAs) play key roles in modulating its function. These ncRNAs interact with p16INK4a through complex post-transcriptional and epigenetic mechanisms, influencing pathways critical to senescence and tumor suppression. In this review, we explore ncRNAs, including ANRIL, MIR31HG, UCA1, MALAT1, miR-24, miR-30, and miR-141, which collectively regulate p16INK4a expression, promoting or inhibiting pathways associated with cancer and aging. ANRIL and MIR31HG modulate p16INK4a silencing via interactions with polycomb repressive complexes (PRC), while miRNAs such as miR-24 and miR-30 target p16INK4a to influence cellular proliferation and senescence. This regulatory interplay underscores the therapeutic potential of ncRNA-targeted strategies to restore p16INK4a function. We summarize recent studies supporting that ncRNAs that control p16INK4a may be diagnostic biomarkers and therapeutic targets for age-related diseases and cancer.

Non-coding RNAs have gathered significant attention for their unique roles in biological regulation. Across a broad spectrum of developmental processes and diseases, particularly in human malignancies, ncRNAs play pivotal roles in regulatory mechanisms. MicroRNAs, long noncoding RNAs, and small nucleolar RNAs stand out among the diverse forms of ncRNAs that have been implicated in cancer. MiRNAs, classified as short non-coding RNAs, modulate gene expression by binding to messenger RNA molecules, thereby inhibiting their translation. Altered miRNA expression has been associated with the onset and progression of various malignancies, including lung, breast, and prostate cancer. In contrast, lncRNAs, characterized as longer ncRNAs, exert control over gene expression through various mechanisms, such as chromatin remodelling and gene silencing. This review offers a comprehensive examination of the numerous ncRNAs that have emerged as crucial regulators of gene expression, playing implicated roles in the initiation and progression of diverse cancers.

Recent studies have found Several lncRNAs were proved differential expression in diminished ovarian reserve (DOR) patients, however, the mechanism of DOR caused by lncRNAs is still largely unclear.

High throughput sequencing was performed in ovarian GCs extracted from women with normal ovarian function and women with DOR. Bioinformation analysis was used to analyze the sequencing data and identify the differential expression of lncRNAs. Quantitative RT-PCR (qRT-PCR) was used to verify the sequencing results. Situ fluorescence hybridization (FISH) followed by confocal microscopy and qRT-PCR were used to explore the location and expression of LncRNA-THBS4 in GCs. The significantly enriched signaling pathways of LncRNA-THBS4 were identified by KEGG. The study used RNA interference technology to decipher LncRNA-THBS4 function by silencing LncRNA-THBS4 in GCs. Western blot and qRT-PCR were used to explore the mRNA and protein expressions of key factors of PI3Ks pathway. The pro-apoptotic protein and anti-apoptotic protein were detected by western blot. The proliferation and apoptosis of GCs were detected by MTT assay and Flow cytometry.

197 lncRNAs with significant differences in expression levels were detected between control and DOR group by high throughput sequencing. The study found the expression of LncRNA-THBS4 in GCs was positively correlated with Anti-Mullerian hormone (AMH) (p = 0.0020, r = 0.4742)、antral follicle count (AFC) (p = 0.0007, r = 0.5130)、good embryo rate (p = 0.0006, r = 0.5210), negatively correlated with basal FSH level (p = 0.0007, r = －0.5152). LncRNA-THBS4 was mainly localized in the cytoplasm of GCs. LncRNA-THBS4 silencing could inhibit the PI3Ks pathway; decrease the levels of anti-apoptotic protein, inhibit the proliferation of GCs; increase the levels of apoptosis protein, enhance the apoptosis of GCs.

The expression level of lncRNA-THBS4 is correlated with ovarian function indicators and pregnancy outcomes in women. LncRNA-THBS4 may participate in the pathogenesis of DOR by affecting the proliferation and apoptosis of GCs via regulating PI3K/AKT/mTOR signaling pathway.

The development of primary liver cancer (hepatocellular carcinoma [HCC] and intrahepatic cholangiocarcinoma [ICC]) is linked to its physical microenvironment, particularly extracellular matrix (ECM) stiffness. Potential anticancer strategies targeting ECM stiffness include prevention/reversal of the stiffening process and disruption of the response of cancer cells to mechanical signals from ECM. However, each strategy has limitations. Therefore, the authors propose integrating them to maximize their strengths. Compared with HCC, ICC has a stiffer ECM and a worse prognosis. Therefore, ICC is selected to investigate mechanisms underlying the influence of ECM stiffness on cancer progression and application of the integrated anticancer strategy targeting ECM stiffness. In summary, immunofluorescence results for 181 primary liver cancer tissue chips (ICC, n = 91; HCC, n = 90) and analysis of TCGA mRNA-sequencing demonstrate that ECM stiffness can affect phenotypes of primary liver cancers. The YAP1/ABHD11-AS1/STAU2/ZYX/p-YAP1 pathway is a useful entry point for exploration of specific mechanisms of mechanical signal conduction from the ECM in ICC cells and their impact on cancer progression. Moreover, a synergistic anticancer strategy targeting ECM stiffness (ICCM@NPs + siABHD11-AS1@BAPN) is constructed by integrating ECM softening and blocking intracellular mechanical signal transduction in ICC and can provide insights for the treatment of cancers characterized by stiff ECM.

Sorbitol is an important primary metabolite that serves as both a carbon source and signal to pathogens. The leaf diseases caused by Alternata alternata are particularly serious in crabapple (Malus micromalus). Here, we found that sorbitol can enhance the resistance of crabapple to A. alternata R1 by increasing the content of flavonoid catechin. Nanomaterials as an emerging technology tool can efficiently deliver lncRNA to target cells. Here, we found nanoencapsulated lncRNA809 (SPc/lncRNA809) exhibits significant resistance to R1strain. To elucidate the effect of SPc/lncRNA809 on flavonoids catechin synthesis, we observed the expression of lncRNA809 was consistent with that of MmNAC17 which regulates the synthesis of catechin and both could jointly respond to sorbitol. MmNAC17 induced the accumulation of catechin in vivo by directly activating the expression of catechin synthase genes MmF3H and MmLAR. Correspondingly, overexpression of lncRNA809 significantly upregulated the expression of MmNAC17 and enhanced the disease resistance. This study reveals for the first time that sorbitol positively regulates the expression of MmNAC17 through lncRNA809, promoting the accumulation of catechin via the expression of MmF3H and MmLAR, ultimately improving the defense response of M. micromalus. This research provides a crucial foundation for the establishment and application of sorbitol-based signaling regulatory networks.

Alternative proteins (AltProts) are a class of proteins encoded by DNA sequences previously classified as noncoding. Despite their historically being overlooked, recent studies have highlighted their widespread presence and distinctive biological roles. So far, direct detection of AltProt has been relying on data-dependent acquisition (DDA) mass spectrometry (MS). However, data-independent acquisition (DIA) MS, a method that is rapidly gaining popularity for the analysis of canonical proteins, has seen limited application in AltProt research, largely due to the complexities involved in constructing DIA libraries. In this study, we present a novel DIA workflow that leverages a fragmentation spectra predictor for the efficient construction of DIA libraries, significantly enhancing the detection of AltProts. Our method achieved a 2-fold increase in the identification of AltProts and a 50% reduction in missing values compared to DDA. We conducted a comprehensive comparison of four AltProt databases, four DIA-library construction strategies, and three analytical software tools to establish an optimal workflow for AltProt analysis. Utilizing this workflow, we investigated the mouse heart development process and identified over 50 AltProts with differential expression between embryonic and adult heart tissues. Over 30 unannotated mouse AltProts were validated, including ASDURF, which played a crucial role in cardiac development. Our findings not only provide a practical workflow for MS-based AltProt analysis but also reveal novel AltProts with potential significance in biological functions.

Long non-coding RNAs (lncRNAs) are critical regulators of physiological and pathological processes, with their dysregulation increasingly implicated in aging and Alzheimer's disease (AD). Using spatial transcriptomics, we analyzed 78 postmortem brain sections from 21 ROSMAP participants to map the spatial expression of lncRNAs in the dorsolateral prefrontal cortex of aged human brains. Compared to mRNAs, lncRNAs exhibited greater subregion-specific expression, with enrichment in antisense and lincRNA biotypes. Network analysis identified 193 gene modules across eight subregions, including lncRNA-enriched modules involved in critical biological processes. We also identified AD differentially expressed (DE) lncRNAs, which showed greater subregion specificity than AD DE mRNAs. Gene set enrichment analysis highlighted the involvement of these AD DE lncRNAs in epigenetic regulation and chromatin remodeling, including enrichment for HDAC target genes such as OIP5-AS1. Statistical modeling suggested that interactions between OIP5-AS1 and HDAC proteins, particularly HDAC11, were associated with tau tangles in excitatory neurons and plaque burden in microglia. This study provides a comprehensive resource of lncRNA spatial expression in the aged human brain and uncovers potential functional roles of lncRNAs in AD pathogenesis.

High-throughput sequencing technologies and innovative bioinformatics tools discovered that most of the genome is transcribed into RNA. However, only a fraction of the RNAs in cell translates into proteins, while the majority of them are categorized as noncoding RNAs (ncRNAs). The ncRNAs with more than 200 nt without protein-coding ability are termed long noncoding RNAs (lncRNAs). Hundreds of studies established that lncRNAs are a crucial RNA family regulating gene expression. Regulatory RNAs, including lncRNAs, modulate gene expression by interacting with RNA, DNA, and proteins. Several databases and computational tools have been developed to explore the functions of lncRNAs in cellular physiology. This chapter discusses the tools available for lncRNA functional analysis and provides a detailed workflow for the computational analysis of lncRNAs.

In the face of global health challenges posed by infectious diseases and the emergence of drug-resistant pathogens, the exploration of cellular non-coding RNA (ncRNA) networks has unveiled new dimensions in infection research. Particularly microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have emerged as instrumental players in ensuring a balance between protection against hyper-inflammatory conditions and the effective elimination of pathogens. Specifically, ncRNAs, such as the miRNA miR-155 or the lncRNAs MaIL1 (macrophage interferon-regulatory lncRNA 1), and LUCAT1 (lung cancer-associated transcript 1) have been recurrently linked to infectious and inflammatory diseases. Together with other ncRNAs, discussed in this chapter, they form a complex regulatory network shaping the host response to pathogens. Additionally, some pathogens exploit these ncRNAs to establish and sustain infections, underscoring their dual roles in host protection and colonization. Despite the substantial progress made, the vast majority of ncRNA loci remains unexplored, with ongoing research likely to reveal novel ncRNA categories and expand our understanding of their roles in infections. This chapter consolidates current insights into ncRNA-mediated regulatory networks, highlighting their contributions to severe diseases and their potential as targets and biomarkers for innovative therapeutic strategies.

Breast cancer remains a leading global health challenge requiring innovative, therapeutic strategies to improve patient outcomes. This review explores the pivotal roles of non-coding RNAs (ncRNAs), including long non-coding RNA, micro RNA, and circular RNA, in breast cancer biology. We highlight how these molecules regulate critical signaling pathways, influence tumor microenvironments, and contribute to treatment resistance. Our findings underscore the potential of ncRNAs as biomarkers for early diagnosis and as treatment targets for personalized treatment strategies. To pave the way for innovative cancer management approaches, we investigate the complex interactions of ncRNAs and their impact on tumor progression. This comprehensive review enhances our understanding of breast cancer biology while emphasizing the translational significance of ncRNA research in developing effective treatment strategies. Additional research and clinical studies are required to confirm the diagnostic and medicinal value of ncRNAs in breast cancer. Investigating the complex networks of ncRNA interactions and their links to other biological pathways can lead to the discovery of new treatment targets. Furthermore, leveraging advanced technologies, such as machine learning and multi-omics methods, will be critical in improving our understanding of ncRNAs biomarkers and translating these insights into impactful clinical applications.

Osteoporosis is well noted to be a universal ailment that realization impaired bone mass and micro architectural deterioration thus enhancing the probability of fracture. Despite its high incidence, its management remains highly demanding because of the multifactorial pathophysiology of the disease. This review highlights recent findings in the management of osteoporosis particularly, gene expression and hormonal control. Some of the newest approaches regarding the subject are described, including single-cell RNA sequencing and long non-coding RNAs. Also, the review reflects new findings on hormonal signaling and estrogen and parathyroid hormone; patient-specific approaches due to genetic and hormonal variation. Potential new biomarkers and AI comprised as factors for improving the ability to anticipate and manage fractures. These hold great potential of new drugs, combination therapies and gene based therapies for osteoporosis in the future. Further studies and cooperation of scientists and clinicians will help to apply such novelties into practical uses in the sphere of medicine in order to enhance the treatment of patients with osteoporosis.

Traumatic brain injury (TBI) poses a major global health challenge, leading to serious repercussions for those affected and imposing considerable financial strains on families and healthcare systems. RNA methylation, especially 5-methylcytosine (m5C), plays a crucial role as an epigenetic modification in regulating RNA at the level of post-transcriptional regulation. However, the impact of TBI on the m5C methylation profile of long non-coding RNAs (lncRNAs) remains unexplored. In the present study, we conducted a thorough transcriptome-wide examination of m5C methylation in lncRNAs in a rat TBI model utilizing MeRIP-Seq. Our results revealed significant differences in the amount and distribution of m5C methylation in lncRNAs between TBI and control groups, indicating profound changes in m5C methylation following TBI. Bioinformatic analyses linked these specifically methylated transcripts to pathways involved in immune response, neural repair, and lipid metabolism, providing insight into possible mechanisms underlying TBI pathology. These findings offer novel perspectives on the post-transcriptional modifications in lncRNA m5C methylation following TBI, which may contribute to understanding the disease mechanisms and developing targeted therapeutic strategies.

Extracellular vesicles (EVs) are lipid bilayer nanoparticles released from all known cells and are involved in cell-to-cell communication via their molecular content. EVs have been found in all tissues and body fluids, carrying a variety of biomolecules, including DNA, RNA, proteins, metabolites, and lipids, offering insights into cellular and pathophysiological conditions. Despite the emergence of EVs and their molecular contents as important biological indicators, it remains difficult to explore EV-mediated biological processes due to their small size and heterogeneity and the technical challenges in characterizing their molecular content. EV-associated small RNAs, especially microRNAs, have been extensively studied. However, other less characterized RNAs, including protein-coding mRNAs, long noncoding RNAs, circular RNAs, and tRNAs, have also been found in EVs. Furthermore, the EV-associated proteins can be used to distinguish different types of EVs. The spectrum of EV-associated RNAs, as well as proteins, may be associated with different pathophysiological conditions. Therefore, the ability to comprehensively characterize EVs' molecular content is critical for understanding their biological function and potential applications in disease diagnosis. Here, we set out to provide an overview of EV-associated RNAs and proteins as well as approaches currently being used to characterize them.

Long noncoding RNA (lncRNA) is a significant component of the noncoding genome and refers to RNA molecules that exceed 200 nucleotides in length. It plays a crucial role in both promoting and suppressing cancer by regulating the proliferation, invasion, and metastasis of tumor cells. We have found a correlation between cancer susceptibility candidate 11 (CASC11) experssion and tumorigenesis development prognosis in a number of studies on tumors. Hence, this meta-analysis was conducted to further investigate the effects of CASC11 expression on clinicopathological features and outcome. Furthermore, CASC11 can act both as a therapeutic target and a cancer biomarker.

We conducted a thorough search of PubMed, Embase, Web of Science, and Cochrane Library to identify all eligible studies until September 20, 2023. These studies examined the potential relationship between the expression levels of CASC11 and survival or the range of pathological feature in cancer patients. The impact of CASC11 expression on overall survival (OS) was evaluated using pooled hazard ratios and 95% confidence intervals (CI). The relationship between CASC11 expression and clinicopathological features was assessed through pooled odds ratios and 95% CI.

A total of 11 studies, involving 660 patients, were examined in this analysis. The results revealed that the overexpression of CASC11 was significantly associated with poor OS (hazard ratios = 2.07, 95%CI = 1.64-2.60) in cancer. Further subgroup analysis demonstrated that the overexpression of CASC11 was consistently linked to poorer OS in diverse types of cancer, including digestive system neoplasm, respiratory neoplasms, and gynecologic tumor.

Overall, this analysis established a strong correlation between CASC11 expression and tumor prognosis, suggesting its potential as a predictive marker for tumor progression in diverse cancer types.

Gallbladder cancer (GBC) is an aggressive and lethal malignancy with a poor prognosis. Long noncoding RNAs (lncRNAs) and natural products have emerged as key orchestrators of cancer pathogenesis through widespread dysregulation across GBC transcriptomes. Functional studies have revealed that lncRNAs interact with oncoproteins and tumor suppressors to control proliferation, invasion, metastasis, angiogenesis, stemness, and drug resistance. Curcumin, baicalein, oleanolic acid, shikonin, oxymatrine, arctigenin, liensinine, fangchinoline, and dioscin are a few examples of natural compounds that have demonstrated promising anticancer activities against GBC through the regulation of important signaling pathways. The lncRNAs, i.e., SNHG6, Linc00261, GALM, OIP5-AS1, FOXD2-AS1, MINCR, DGCR5, MEG3, GATA6-AS, TUG1, and DILC, are key players in regulating the aforementioned processes. For example, the lncRNAs FOXD2-AS1, DILC, and HOTAIR activate oncogenes such as DNMT1, Wnt/β-catenin, BMI1, and c-Myc, whereas MEG3 and GATA6-AS suppress the tumor proteins NF-κB, EZH2, and miR-421. Clinically, specific lncRNAs can serve as diagnostic or prognostic biomarkers based on overexpression correlating with advanced TNM stage, metastasis, chemoresistance, and poor survival. Therapeutically, targeting aberrant lncRNAs with siRNA or antisense oligos disrupts their oncogenic signaling and inhibits GBC progression. Overall, dysfunctional lncRNA regulatory circuits offer multiple avenues for precision medicine approaches to improve early GBC detection and overcome this deadly cancer. They have the potential to serve as novel biomarkers as they are detectable in bodily fluids and tissues. These findings enhance gallbladder treatments, mitigating resistance to chemo- and radiotherapy.

Prostate cancer stands as the most common cancer in men, and research into its genesis and spread is still vital. The idea that the human genome's transcriptional activity is more widespread than previously thought has received empirical validation through the application of deep sequencing-based transcriptome profiling techniques. An assortment of noncoding transcripts longer than 200 nucleotides is referred to as long noncoding RNAs (lncRNAs). Transposable elements comprise a substantial portion of the human genome, with projections indicating that their prospective proportion may reach 90%. Considering they can interact directly with proteins, alter the transcriptional activity of coding genes, and perhaps encode proteins, lncRNAs possess the capability to regulate a variety of biological processes. LncRNAs have been recognized to be key factors in the development of several types of human cancers, including lung, colorectal, and breast cancers, alongside other pathological processes that have a significant impact on the diagnosis and survival of cancer individuals. Furthermore, lncRNAs' discernible expression patterns throughout various cancer scenarios significantly raise their potential as biomarkers and therapeutic targets. We conducted an extensive analysis of the prevailing academic literature on the interaction between lncRNAs and prostate cancer in order to present a solid foundation for potential future studies on the prevention and intervention of prostate cancer. The discourse additionally expands on lncRNAs' prospective applications as targets and biomarkers for medical therapies.

Cancer remains a major global health concern with high mortality rates mainly due to late diagnosis and poor prognosis. Long non-coding RNAs (lncRNAs) are emerging as key regulators of gene expression in human cancer, functioning through various mechanisms including as competing endogenous RNAs (ceRNAs) and indirectly regulating miRNA expression. LncRNAs have been found to have both oncogenic and tumor-suppressive roles in cancer, with the former promoting cancer cell proliferation, migration, invasion, and poor prognosis. Recent research has shown that lncRNAs are expressed in various immune cells and are involved in cancer cell immune escape and the modulation of the tumor microenvironment, thus highlighting their potential as targets for cancer immunotherapy. Targeting lncRNAs in cancer or immune cells could enhance the anti-tumor immune response and improve cancer immunotherapy outcomes. However, further research is required to fully understand the functional roles of lncRNAs in cancer and the immune system and their potential as targets for cancer immunotherapy. This review offers a comprehensive examination of the multifaceted roles of lncRNAs in human cancers, with a focus on their potential as targets for cancer immunotherapy. By exploring the intricate mechanisms underlying lncRNA-mediated regulation of cancer cell proliferation, invasion, and immune evasion, we provide insights into the diverse therapeutic applications of these molecules.

Recent studies of noncoding genomes have shown important implications for regulating gene expression and genetic programs during development and their association with health, including cardiovascular disease. There are nearly 2,500 microRNAs (miRNAs), 12,000 long-chain non-coding RNAs (lncRNA), and nearly 4,000 circular RNAs (circles). Even though they do not code for proteins, they make up nearly 99% of the human genome. Non-coding RNA families (ncRNAs) have recently been discovered and established as novel and necessary controllers of cardiovascular risk factors and cellular processes and, therefore, have the potential to improve the diagnosis and prediction of cardiovascular disease. The increase in the prevalence of cardiovascular disease can be explained by the shortcomings of existing therapies, which focus only on the non-coding RNAs that protein codes for. On the other hand, recent studies point to the possibility of using ncRNAs in the early detection and intervention of CVD. These findings suggest that developing diagnostic tools and therapies based on miRNAs, lncRNAs, and circRNAs will potentially enhance the clinical management of patients with cardiovascular disease. Cardiovascular diseases include CH, HF, RHD, ACS, MI, AS, MF, ARR, and PAH, of which CH is the most common cardiovascular disease, followed by HF and RHD. This paper aims to elucidate the biological and clinical significance of miRNAs, increase, and circles, as well as their expression profiles and the possibility of regulating non-coding transcripts in cardiovascular diseases to improve the application of ncRNAs in diagnosis and treatment.

Pancreatic cancer (PaC) incidence is increasing, but our current screening and diagnostic strategies are not very effective. However, screening could be helpful in the case of PaC, as recent evidence shows that the disease progresses gradually. Unfortunately, there is no ideal screening method or program for detecting PaC in its early stages. Conventional imaging techniques, such as abdominal ultrasound, CT, MRI, and EUS, have not been successful in detecting early-stage PaC. On the other hand, biomarkers may be a more effective screening tool for PaC and have greater potential for further evaluation compared to imaging. Recent studies on biomarkers and artificial intelligence (AI)-enhanced imaging have shown promising results in the early diagnosis of PaC. In addition to proteins, non-coding RNAs are also being studied as potential biomarkers for PaC. This review consolidates the current literature on PaC screening modalities to provide an organized framework for future studies. While conventional imaging techniques have not been effective in detecting early-stage PaC, biomarkers and AI-enhanced imaging are promising avenues of research. Further studies on the use of biomarkers, particularly non-coding RNAs, in combination with imaging modalities may improve the accuracy of PaC screening and lead to earlier detection of this deadly disease.

T-cell Acute Lymphoblastic Leukemia (T-ALL) is a highly aggressive form of ALL with at least 25% relapse rates. The high relapse rates are often linked to poor prognoses. More detailed studies for novel therapeutic targets for the treatment of T-ALL are required as the genetic and transcriptomic data currently available on T-ALL pathophysiology is insufficient. Long non-coding RNAs are emerging as important players in the regulation of tumour proliferation and metastasis. Studies on various cancers have revealed their potential as biomarkers and therapeutic targets in treatment. This review describes the characterization, biosynthesis, and role of long non-coding RNA in T-ALL and highlights their potential as next generation molecule in development of promising diagnostic, prognostic and/or therapeutic markers.

Obesity has escalated into a critical global health crisis, tripling in prevalence since the mid-1970s. This increase mirrors the rise in metabolic-associated diseases such as type 2 diabetes (T2D) and its complications, certain cancers, and cardiovascular conditions. While substantial research efforts have enriched our understanding and led to the development of innovative management strategies for these diseases, the suboptimal response rates of existing therapies remain a major obstacle to effectively managing obesity and its associated conditions. Over the years, inter-organ communication (IOC) has emerged as a crucial factor in the development and progression of metabolic disorders. Exosomes, which are nano-sized vesicular couriers released by cells, play a significant role in this communication by transporting proteins, lipids, and nucleic acids across cellular landscapes. The available evidence indicates that exosomal RNAs present in biofluids such as blood, urine, milk, vitreous humor (VH), and cerebrospinal fluid (CSF) are altered in numerous diseases, suggesting their diagnostic and therapeutic potential. Long non-coding RNAs contained in exosomes (exo-lncRNAs) have attracted considerable interest, owing to their ability to interact with critical components involved in a multitude of metabolic pathways. Recent studies have found that alterations in exo-lncRNAs in biofluids correlate with several metabolic parameters in patients with metabolic-associated conditions; however, their exact roles remain largely unclear. This review highlights the diagnostic and therapeutic potential of exosomal lncRNAs in obesity and its associated conditions, emphasizing their role in IOC and disease progression, aiming to pave the way for further research in this promising domain.

Long non-coding RNA (lncRNA) refers to an RNA molecule longer than 200 nucleotides (nt) that plays a significant role in regulating essential molecular and biological processes. It is commonly found in animals, plants, and viruses, and is characterized by features such as epigenetic markers, developmental stage-specific expression, and tissue-specific expression. Research has shown that lncRNA participates in anatomical processes like plant progression, while also playing a crucial role in plant disease resistance and adaptation mechanisms. In this review, we provide a concise overview of the formation mechanism, structural characteristics, and databases related to lncRNA in recent years. We primarily discuss the biological roles of lncRNA in plant progression as well as its involvement in response to biotic and abiotic stresses. Additionally, we examine the current challenges associated with lncRNA and explore its potential application in crop production and breeding. Studying plant lncRNAs is highly significant for multiple reasons: It reveals the regulatory mechanisms of plant growth and development, promotes agricultural production and food security, and drives research in plant genomics and epigenetics. Additionally, it facilitates ecological protection and biodiversity conservation.

Endothelial-mesenchymal transformation (EndoMT) is the process through which endothelial cells transform into mesenchymal cells, affecting their morphology, gene expression, and function. EndoMT is a potential risk factor for cardiovascular and cerebrovascular diseases, tumor metastasis, and fibrosis. Recent research has highlighted the role of exosomes, a mode of cellular communication, in the regulation of EndoMT. Exosomes from diseased tissues and microenvironments can promote EndoMT, increase endothelial permeability, and compromise the vascular barrier. Conversely, exosomes derived from stem cells or progenitor cells can inhibit the EndoMT process and preserve endothelial function. By modifying exosome membranes or contents, we can harness the advantages of exosomes as carriers, enhancing their targeting and ability to inhibit EndoMT. This review aims to systematically summarize the regulation of EndoMT by exosomes in different disease contexts and provide effective strategies for exosome-based EndoMT intervention.