A Non-Coding RNA Network Involved in KSHV Tumorigenesis.
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ABSTRACT:
SUBMITTER: Naipauer J
PROVIDER: S-EPMC8242244 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:In our study, we aimed to reveal potential long non-coding RNAs (lncRNA) biomarkers in lung adenocarcinoma (LAD) using lncRNA-mediated competing endogenous RNAs (ceRNAs) network (LMCN). Competing lncRNA-mRNA interactions were identified using the hypergeometric test. Co-expression analysis for the competing lncRNA-mRNA interactions was implemented, and relying on the weight value >0.8, a highly competitive LMCN was further constructed. Degree distribution, betweenness and closeness for LMCN were carried out to analyze the network structure. Functional analyses of mRNAs in LMCN were carried out to further explore the biological functions of lncRNAs. Biclique algorithm was utilized to extract competing modules from the LMCN. Finally, we verified our findings in an independent sample set using qRT-PCR. Based on degrees >60, we identified 4 hubs, including DLEU2, SNHG12, HCP5, and LINC00472. Furthermore, 2 competing modules were identified, and LINC00472 in module 1 functioned as a hub in both LMCN and module. Functional implications of lncRNAs demonstrated that lncRNAs were related to histone modification, negative regulation of cell cycle, neuroactive ligand-receptor interaction, and regulation of actin cytoskeleton. qRT-PCR results demonstrated that lncRNAs LINC00472, and HCP5 were down-regulated in LAD tissues, while the expression level of SNHG12 was up-regulated in LAD tissues. Our study sheds novel light on the roles of lncRNA-related ceRNA network in LAD and facilitates the detection of potential lncRNA biomarkers for LAD diagnosis and treatment. Remarkably, in our study, LINC00472, HCP5, and SNHG12 might be potential biomarkers for LAD management.
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Project description:Although accumulating evidence has provided insight into the various functions of long-non-coding RNAs (lncRNAs), the exact functions of the majority of such transcripts are still unknown. Here, we report the first computational annotation of lncRNA functions based on public microarray expression profiles. A coding-non-coding gene co-expression (CNC) network was constructed from re-annotated Affymetrix Mouse Genome Array data. Probable functions for altogether 340 lncRNAs were predicted based on topological or other network characteristics, such as module sharing, association with network hubs and combinations of co-expression and genomic adjacency. The functions annotated to the lncRNAs mainly involve organ or tissue development (e.g. neuron, eye and muscle development), cellular transport (e.g. neuronal transport and sodium ion, acid or lipid transport) or metabolic processes (e.g. involving macromolecules, phosphocreatine and tyrosine).
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Project description:BackgroundLong non-coding RNAs (lncRNAs) are not translated into proteins and were initially considered to be part of the 'dark matter' of the genome. Recently, it has been shown that lncRNAs play a role in the recruitment of chromatin modifying complexes and can influence gene expression. However, it is unknown if lncRNAs function in a similar way in cancer.ResultsHere, we show that the lncRNA ROR occupies and activates the TESC promoter by repelling the histone G9A methyltransferase and promoting the release of histone H3K9 methylation. Suppression of ROR in tumors results in silencing of TESC expression, and G9A-mediated histone H3K9 methylation in the TESC promoter is restored, which significantly reduces tumor growth and metastasis. Without ROR silencing, TESC knockdown presents consistent and significant reductions in tumor progression.ConclusionsOur results reveal a novel mechanism by which ROR may serve as a decoy oncoRNA that blocks binding surfaces, preventing the recruitment of histone modifying enzymes, thereby specifying a new pattern of histone modifications that promote tumorigenesis.
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Project description:Recently, long non-coding RNAs (lncRNAs) have been reported as the vital regulators of various cancers including nasopharyngeal carcinoma (NPC). An increasing number of studies have suggested that lncRNA LINC01133 is dysregulated and involved in human carcinogenesis. However, the roles of LINC01133 in NPC remain largely unknown. In this work, we demonstrated that LINC01133 was significantly downregulated in NPC tissues and cell lines. Loss and gain of function experiments provided evidence that LINC01133 inhibited NPC cell proliferation, invasion and migration both in vitro and in vivo. Besides, Fluorescence in situ hybridization (FISH) assay was performed to determine the localization of LINC01133 and LINC01133 was observed mainly distributed in the nucleus. Importantly, RNA pull-down and RIP assays showed that LINC01133 directly combined with YBX1, and YBX1 can partly reverse the repression of NPC cell proliferation, migration, and invasion caused by LINC01133. Collectively, our exploration indicate that LINC01133 inhibits the malignant-biological behavior of NPC cells by binding to YBX1, thereby suggesting a novel biomarker for the NPC prognosis and treatment.
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Project description:Breast cancer is one of the most common malignant tumors in women and is the second leading cause of cancer deaths among women. The tumorigenesis and progression of breast cancer are not well understood. The existing researches have indicated that non-coding RNAs, which mainly include long non-coding RNA (lncRNA) and microRNA (miRNA), have gradually become important regulators of breast cancer. We aimed to screen the differential expression of miRNA and lncRNA in the different breast cancer stages and identify the key non-coding RNA using TCGA data. Based on series test of cluster (STC) analysis, bioinformatics analysis, and negatively correlated relationships, 122 lncRNAs, 67 miRNAs, and 119 mRNAs were selected to construct the regulatory network of lncRNA and miRNA. It was shown that the miR-93/20b/106a/106b family was at the center of the regulatory network. Furthermore, 6 miRNAs, 10 lncRNAs, and 15 mRNAs were significantly associated with the overall survival (OS, log-rank P < 0.05) of patients with breast cancer. Overexpressed miR-93 in MCF-7 breast cancer cells was associated with suppressed expression of multiple lncRNAs, and these downregulated lncRNAs (MESTIT1, LOC100128164, and DNMBP-AS1) were significantly associated with poor overall survival in breast cancer patients. Therefore, the miR-93/20b/106a/106b family at the core of the regulatory network discovered by our analysis above may be extremely important for the regulation of lncRNA expression and the progression of breast cancer. The identified key miRNA and lncRNA will enhance the understanding of molecular mechanisms of breast cancer progression. Targeting these key non-coding RNA may provide new therapeutic strategies for breast cancer treatment and may prevent the progression of breast cancer from an early stage to an advanced stage.
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Project description:nc886 (= vtRNA2-1 or pre-miR-886) is a recently discovered noncoding RNA that is a cellular PKR (Protein Kinase RNA-activated) ligand and repressor. nc886 has been suggested to be a tumor suppressor, solely based on its expression pattern and genomic locus. In this report, we have provided sufficient evidence that nc886 is a putative tumor suppressor in esophageal squamous cell carcinoma (ESCC). In 84 paired specimens from ESCC patients, nc886 expression is significantly lower in tumors than their normal adjacent tissues. More importantly, decreased expression of nc886 is significantly associated with shorter recurrence-free survival of the patients. Suppression of nc886 is mediated by CpG hypermethylation of its promoter, as evidenced by its significant negative correlation to nc886 expression in ESCC tumors and by induced expression of nc886 upon demethylation of its promoter. Knockdown of nc886 and consequent PKR activation induce FOS and MYC oncogenes as well as some inflammatory genes including oncogenic NF-?B. When ectopically expressed, nc886 inhibits proliferation of ESCC cells, further demonstrating that nc886 could be a tumor suppressor. All these findings implicate nc886 as a novel, putative tumor suppressor that is epigenetically silenced and regulates the expression of oncogenes in ESCC.
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Project description:Long non-coding RNAs are a kind of endogenous ncRNAs with a length of more than 200 bp. Accumulating evidence suggests that long non-coding RNAs function as pivotal regulators in tumorigenesis and progression. However, their biological roles in breast cancer remain largely unknown. Here, we found that IGF2 antisense RNA (IGF2-AS) was significantly decreased in breast cancer tissues, cell lines, and plasma. Patients with low IGF2-AS were more likely to develop larger tumor size and later clinical stage. Overexpression of IGF2-AS evidently inhibited the proliferation and induced apoptosis of MCF-7 and T47D cells in vitro, as well as retarded tumor growth in vivo. Further investigation revealed that IGF2-AS inhibited the expression of its sense-cognate gene IGF2 in an epigenetic DNMT1-dependent manner, resulting in the inactivation of downstream oncogenic PI3K/AKT/mTOR signaling pathway. Enforced expression of IGF2 could significantly block the tumor inhibitory effect of IGF2-AS. Importantly, we found that IGF2-AS could be used as an effective biomarker for breast cancer diagnosis and prognosis. Taken together, our study indicates that IGF2-AS is a tumor suppressor in breast cancer, restoration of IGF2-AS may be a promising treatment for this fatal disease.
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