• Colorectal cancer
• Ferroptosis
• LncRNA FTX
• Radioresistance
• Redox
• Solute carrier family 7 member 11

• Humans
• Ferroptosis/genetics
• Ferroptosis/radiation effects
• Colorectal Neoplasms/radiotherapy
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/pathology
• MicroRNAs/metabolism
• MicroRNAs/genetics
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Animals
• Radiation Tolerance/genetics
• Mice
• Gene Expression Regulation, Neoplastic/radiation effects
• Amino Acid Transport System y+/metabolism
• Amino Acid Transport System y+/genetics
• Oxidation-Reduction/radiation effects
• HT29 Cells
• HCT116 Cells
• Xenograft Model Antitumor Assays
• Reactive Oxygen Species/metabolism
• Up-Regulation
• Cell Survival/radiation effects
• Gene Knockdown Techniques

• Colorectal Cancer (CRC)
• In silico
• LncRNA
• Non-invasive biomarkers
• Precision medicine
• Signaling pathways
• ncRNA

• Humans
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/pathology
• Colorectal Neoplasms/therapy
• RNA, Long Noncoding/genetics
• Precision Medicine/methods
• Gene Expression Regulation, Neoplastic
• Epithelial-Mesenchymal Transition/genetics
• Epigenesis, Genetic
• Animals
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Prognosis

• Colorectal cancer
• Invasion
• Migration
• Prognosis
• lncRNA LINC01128
• miR-363-3p

• Humans
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/pathology
• RNA, Long Noncoding/genetics
• MicroRNAs/genetics
• Prognosis
• Male
• Cell Proliferation/genetics
• Female
• Middle Aged
• Up-Regulation
• Gene Expression Regulation, Neoplastic
• Cell Line, Tumor
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Lymphatic Metastasis/genetics
• Aged

• 20231800935592 Dongguan Science and Technology of Social Development Program
• YB201915 Jiangsu Province Traditional Chinese Medicine Technology Development Plan Project
• Guozhongyao Renjiao Han [2022] No. 76 The seventh batch of national experts in traditional Chinese medicine academic experience inheritance work

• LINC01485
• colorectal cancer
• keratin 80
• miR-383-5p

• Humans
• Carcinogenesis/genetics
• Carcinogenesis/pathology
• Cell Line, Tumor
• Cell Proliferation/genetics
• Colorectal Neoplasms/metabolism
• MicroRNAs/genetics
• MicroRNAs/metabolism
• RNA, Long Noncoding/genetics
• Keratins, Type II/genetics

• WX21Z35 Western Medicine and Public Health Scientific Research Projects of Wuhan Municipal Health Commission

• Biomarkers
• Cancer
• FTX
• LncRNAs
• miRNAs

• Female
• Humans
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Glycogen Synthase Kinase 3 beta/metabolism
• Phosphatidylinositol 3-Kinases/metabolism
• MicroRNAs/genetics
• Signal Transduction/genetics
• SOXC Transcription Factors/metabolism

• CTNNBIP1
• colorectal cancer
• miR-3194-5p
• paeoniflorin
• stemness

• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Cell Line, Tumor
• beta Catenin/genetics
• beta Catenin/metabolism
• Colorectal Neoplasms/drug therapy
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/metabolism
• Cell Proliferation/genetics
• Gene Expression Regulation, Neoplastic
• Cell Movement/genetics

• 202028 Key projects supported by Hunan Administration of Traditional Chinese Medicine
• 21A0223 Key projects supported by Hunan Provincial Department of Education
• kq1907118 Supported by Changsha Natural Science Foundation

• LINCRNA
• M6a modification
• Ovarian cancer(oc)
• chemoresistant

• Humans
• Female
• Ovarian Neoplasms/pathology
• Ovarian Neoplasms/metabolism
• Ovarian Neoplasms/drug therapy
• Ovarian Neoplasms/genetics
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• Cell Movement
• Cell Line, Tumor
• Paclitaxel/pharmacology
• Drug Resistance, Neoplasm
• Adenosine/analogs & derivatives
• Adenosine/metabolism
• Gene Expression Regulation, Neoplastic
• Cell Proliferation
• Neoplasm Invasiveness
• TOR Serine-Threonine Kinases/metabolism

• Anti-EGFR resistance
• Colorectal cancer
• EGFR
• LncRNAs
• Targeting therapy

• BAMBI
• Colorectal cancer
• Metastasis
• SP5
• circSP5

• Animals
• Humans
• Colorectal Neoplasms/genetics
• Disease Models, Animal
• Liver Neoplasms/genetics
• Membrane Proteins
• RNA
• RNA, Circular/genetics

• 82103439 the National Natural Science Foundation of China

• ADM
• Acinar Cells
• PDAC

• Animals
• Humans
• Mice
• Acinar Cells/metabolism
• Acute Disease
• Carcinoma in Situ/metabolism
• Carcinoma, Pancreatic Ductal/pathology
• Immunoglobulin J Recombination Signal Sequence-Binding Protein/genetics
• Immunoglobulin J Recombination Signal Sequence-Binding Protein/metabolism
• Mice, Transgenic
• Pancreatic Neoplasms/pathology
• Pancreatitis/pathology
• Proto-Oncogene Proteins p21(ras)/genetics
• Proto-Oncogene Proteins p21(ras)/metabolism

• diabetes
• high glucose
• huvecs
• lncrna
• n6-methyladenosine
• tnf-α

• Animals
• Humans
• RNA, Long Noncoding/genetics
• Tumor Necrosis Factor-alpha/genetics
• Gene Regulatory Networks
• Human Umbilical Vein Endothelial Cells/metabolism
• MicroRNAs/genetics
• RNA, Messenger/metabolism
• Glucose/pharmacology
• Mammals/genetics
• Mammals/metabolism

• Humans
• Female
• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/drug therapy
• Colorectal Neoplasms/genetics
• RNA, Long Noncoding/genetics
• Prognosis
• Biomarkers, Tumor/genetics
• Gene Expression Regulation, Neoplastic

As reported, multiple circular RNAs (circRNAs) interfere with colorectal cancer (CRC) progression. Here, circRNA_0001658 (circ_0001658) is focused on studying how it works in CRC.

Clarify the expression pattern, biological function, and underlying mechanism of circ_0001658 of CRC tumorigenesis.

In CRC-related chip data retrieved using the database named Gene Expression Omnibus, different expressions of circRNAs between CRC and normal tissue samples were identified. Quantitative Real-time PCR and Western blot ensured the analysis on circ_0001658, microRNA-590-5P (miR-590-5p), and methyltransferase-like 3 (METTL3) mRNA expressions in tissues and cells. Cell counting kit-8 and flow cytometry were used to detect cell proliferation, apoptosis and migration. The targeting relations between circ_0001658, miR-590-5p, and METTL3 mRNA 3'-untranslated region were under the verification of bioinformatics prediction and dual luciferase-based reporter gene assays. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were employed on the downstream targets of miR-590-5p using the Database for Annotation, Visualization and Integrated Discovery database.

Circ_0001658 and METTL3 mRNA was elevated in CRC tissues and cells, whereas miR-590-5p was decreased. Circ_0001658 overexpression promoted the proliferation of HT29 cells, inhibited apoptosis, and accelerated the cell cycle. In SW480 cells, knocking down circ_0001658 had the opposite effect. Circ_0001658 could specifically bind to miR-590-5p and negatively modulate its expressions; METTL3 is a miR-590-5p target that can be positively regulated by circ 0001658. Circ 0001658 was inversely associated with miR-590-5p expression while positively with METTL3 expressions.

Circ_0001658 regulates the miR-590-5p/METTL 3-axis to increase CRC cell growth and decrease apoptosis.

• Circ_0001658
• miR-590-5p
• METTL3
• Colorectal cancer
• Proliferation

Background: Colorectal cancer (CRC) is a common malignant tumor that affects the large bowel or the rectum. Cuproptosis, recently discovered programmed cell death process, may play an important role in CRC tumorigenesis. Long non-coding RNAs (lncRNAs) can alter the proliferation of colorectal cancer cells through the control and activation of gene expression. To date, cuproptosis-related lncRNAs, have not been investigated as potential predictive biomarkers in colorectal cancer.

Methods: The mRNA and lncRNA expression data of colorectal cancer were gathered from The Tumor Genome Atlas (TCGA) database, and Pearson correlation analysis and univariate Cox regression analysis were used to identify the lncRNAs with differential prognosis. Colorectal cancer was classified using consistent clustering, and the clinical significance of different types, tumor heterogeneity, and immune microenvironment differences was investigated. The differential lncRNAs were further screened using LASSO regression to develop a risk scoring model, which was then paired with clinicopathological variables to create a nomogram. Finally, the copy number changes in the high-risk and low-risk groups were compared.

Results: Two clusters were formed based on the 28 prognostic cuproptosis-related lncRNAs, and the prognosis of cluster 2 was found to be significantly lower than that of cluster 1. Cluster 1 showed increased immune cell infiltration and immunological score, as well as strong enrichment of immune checkpoint genes. Next, LASSO regression was used to select 11 distinctive lncRNAs, and a risk score model was constructed using the training set to distinguish between high and low-risk groups. Patients in the high-risk group had a lower survival rate than those in the low-risk group, and both the test set and the total set produced consistent results. The AUC value of the ROC curve revealed the scoring model’s efficacy in predicting long-term OS in patients. Moreover, the model could be used as an independent predictor when combined with a multivariate analysis of clinicopathological features, and our nomogram could be used intuitively to predict prognosis.

Conclusion: Collectively, we developed a risk model using 11 differential lncRNAs and demonstrated that the model has predictive value as well as clinical and therapeutic implications for predicting prognosis in CRC patients.

• Osteosarcoma (OS)
• biomarker
• lncRNA
• prognosis

To explore the expression of circular RNA (circRNA) in gastrointestinal stromal tumors.

Gastrointestinal stromal tumors (GIST) are mainly distributed in the stomach and small intestine. Recently, it has been verified that circular RNA (circRNA) has an important function in the regulation of GIST. Nevertheless, detailed investigations of circRNA-miRNA-mRNA regulatory networks in GIST are lacking.

To analyze the gastrointestinal stromal tumor circRNA-miRNA-mRNA network, assessing the effect of circle RNA in gastrointestinal stromal tumors.

All the differential circRNAs and mRNAs were obtained from Gene Expression Omnibus (GEO) microarray data (GSE131481 and GSE147303, GSE131481, and GSE13861). Furthermore, a circRNA-miRNA-mRNA network was established. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment were used to reveal the correlation between the functions of signaling pathways and target genes. The hub genes of protein-protein interaction (PPI) network and cytoHubba were also defined. Quantitative real-time PCR (qRT-PCR) was used to measure the expression levels of hsa-circ-0002917 (circTBC1D4), hsa-miR-590-5p (miR-590-5p), and PLN.

PPI network and Cytoscape showed that ATP1A2, PLN, KCNMA1, and SCNN1B were four central DEGs. GO analysis results revealed that DEGs were involved in negative management of myocardial contraction, regulation of myocardial cell contraction, ethanol oxidation, cellular potassium ion homeostasis, and relaxation of cardiac muscle, and KEGG analysis showed that major DEGs were with cGMP-PKG signaling pathway. Moreover, we obtained two pairs of axes, namely, hsa-circ-0039216/hsa-miR-338-3p/ATP1A2 and hsa-circ-0002917/hsa-miR-590-5p/PLN. The target of TBC1D4 is miR-590-5p, and miR-590-5p increased after knocking down TBC1D4. Moreover, PLN was the target of miR-590-5p, and miR-590-5p exerts antitumor effects by reducing PLN.

In this study, we constructed a circRNA-miRNA-mRNA management network interrelated with GIST and researched the potential roles of circRNA. Moreover, we discovered a new molecular landmarker for the prediction, diagnosis, and therapy of patients.

• Cell Line, Tumor
• Cisplatin/pharmacology
• Drug Resistance, Neoplasm/genetics
• Female
• Forkhead Transcription Factors
• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Ovarian Neoplasms/drug therapy
• Ovarian Neoplasms/genetics
• Ovarian Neoplasms/metabolism

Heterogeneity of breast cancer (BRCA) is significantly correlated with its prognosis. Target therapy for ferroptosis and immunity is a new cancer treatment option discovered in recent years. In the present study, we aimed to identify ferroptosis- and immune-related long non-coding RNAs (lncRNAs) to accurately predict the prognosis and diagnosis of patients with breast infiltrating duct and lobular carcinoma by integrated analyses.

The corresponding data for the patients with breast infiltrating duct and lobular carcinoma by integrated analyses were obtained from The Cancer Genome Atlas (TCGA). Analyses of univariate and multivariate Cox regressions were used to identify the suitable candidate biomarkers.

We found that seven ferroptosis- and immune-related differentially expressed lncRNAs (FI-DELs) (AC007686.3, AC078883.1, ADAMTS9-AS1, AL035661.1, CBR3-AS1, FTX, and TMEM105) were correlated with the overall survival of patients with breast infiltrating duct and lobular carcinoma. The areas under the receiver operating characteristic (AUCs) value of the prognosis model were all over 0.6 in training, validation, and entire groups. The sensitivity and specificity of the diagnosis model was 87.84% and 97.06%, respectively.

Through a series of bioinformatics analyses, we found that the seven FI-DELs could serve as prognostic and diagnostic biomarkers for patients with breast infiltrating duct and lobular carcinoma. However, whether these seven biomarkers could be really applied to the clinic requires further investigations.

• breast infiltrating duct and lobular carcinoma
• diagnosis
• ferroptosis
• immune
• lncRNAs
• prognosis

• Shikonin
• autophagy
• colorectal cancer
• guanine nucleotide binding protein beta polypeptide 1
• microrna-545-3p

• Autophagy/genetics
• Carcinogenesis/genetics
• Cell Line, Tumor
• Cell Proliferation/genetics
• Colonic Neoplasms/genetics
• Colorectal Neoplasms/metabolism
• GTP-Binding Protein beta Subunits/genetics
• Gene Expression Regulation, Neoplastic
• Humans
• MicroRNAs/genetics
• Naphthoquinones

Canine mammary tumor (CMT) is the most common tumor in canines after skin tumors. Long noncoding RNAs (lncRNAs) have crucial roles in human breast tumor initiation and progression, but the role of lncRNAs in canine mammary tumors is unclear. We analyzed the expression profiles of canine mammary tumors and their adjacent non-neoplastic tissue to explore abnormally expressed lncRNAs. LncRNA expression was detected by qRT–PCR. After overexpression of lnc40589 and knockdown of lnc34977 in CMT cells, CCK-8, colony formation, wound healing and Transwell assays were used to assess the proliferation, migration and invasive ability of canine mammary tumor cells. We also established a mammary tumor-bearing nude mouse model. GO analysis and KEGG pathway analysis demonstrated that the differentially expressed lncRNAs were closely related to the mammary tumor. lnc40589 was significantly upregulated and lnc34977 was significantly downregulated in CMTs. In addition, lnc40589 inhibits cell proliferation, migration and invasion, while lnc34977 promotes cell proliferation, migration and invasion. In addition, lnc34977 promotes the development of mammary tumors in animals. Taken together, our study results reveal the lncRNA expression profiles in CMTs and indicate that lnc34977 promotes the development of CMT both in cell culture and in vivo.

Non-coding RNAs (ncRNAs) constitute the majority of the transcriptome, as the result of pervasive transcription of the mammalian genome. Different RNA species, such as lncRNAs, miRNAs, circRNA, mRNAs, engage in regulatory networks based on their reciprocal interactions, often in a competitive manner, in a way denominated “competing endogenous RNA (ceRNA) networks” (“ceRNET”): miRNAs and other ncRNAs modulate each other, since miRNAs can regulate the expression of lncRNAs, which in turn regulate miRNAs, titrating their availability and thus competing with the binding to other RNA targets. The unbalancing of any network component can derail the entire regulatory circuit acting as a driving force for human diseases, thus assigning “new” functions to “old” molecules. This is the case of XIST, the lncRNA characterized in the early 1990s and well known as the essential molecule for X chromosome inactivation in mammalian females, thus preventing an imbalance of X-linked gene expression between females and males. Currently, literature concerning XIST biology is becoming dominated by miRNA associations and they are also gaining prominence for other lncRNAs produced by the X-inactivation center. This review discusses the available literature to explore possible novel functions related to ceRNA activity of lncRNAs produced by the X-inactivation center, beyond their role in dosage compensation, with prospective implications for emerging gender-biased functions and pathological mechanisms.

• Klinefelter syndrome
• Turner syndrome
• X chromosome inactivation
• ceRNET
• lncRNA
• microRNA

Long non-coding RNA (lncRNA) five prime to Xist (FTX) exerts important functions in human cancer, while its role in retinoblastoma (RB) remains unclear. This study aimed to investigate the role of FTX in RB. The expression levels of FTX were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was evaluated by cell counting kit-8 (CCK-8), 5‐ethynyl‐2′‐deoxyuridine (EdU) staining and colony formation assays. Cell migration and invasion were detected by Transwell assay. The relationship among FTX, microRNA-320a (miR-320a) and with-no-lysine kinase 1 (WNK1) was also investigated. In the present study, we found that the expression levels of FTX were notably elevated in RB tissues and cancer cell lines. Overexpression of FTX exacerbated the aggressive phenotypes (cell proliferation, migration and invasion) of RB cells. Downregulation of miR-320a obviously attenuated the inhibitory effects of knockdown of FTX in RB malignant phenotypes, and knockdown of WNK1 also reversed the impacts of miR-320a inhibitor on malignant phenotypes. In vivo experiments further confirmed that knockdown of FTX efficiently prevents tumor growth in vivo. Our results revealed that FTX promoted RB progression by targeting the miR-320a/WNK1 axis (graphical abstract), suggesting that FTX might be a novel therapeutic target for RB.

• FTX
• Retinoblastoma
• WNK1
• miR-320a