Dataset Information

Long non-coding RNA LINC01426 facilitates glioblastoma progression via sponging miR-345-3p and upregulation of VAMP8.

ABSTRACT: Background:Long non-coding RNAs (lncRNAs) has been extensively reported play important roles in regulating the development and progression of cancers, including Glioblastoma (GBM). LINC01426 is a novel lncRNA that has been identified as an oncogenic gene in GBM. Herein, we attempted to elucidate the detailed functions and underlying mechanisms of LINC01426 in GBM. Methods:LINC01426 expression in GBM cell lines and tissues were detected by quantitative real-time PCR (qRT-PCR). Cell Counting Kit-8 (CCK8) assays, colony formation assays, subcutaneous tumor formation assays were utilized to investigate the biological functions of LINC01426 in GBM. Dual-luciferase reporter assays, RNA immunoprecipitation (RIP) and bioinformatic analysis were performed to determine the underlying mechanisms. Results:LINC01426 is up-regulated in malignant GBM tissues and cell lines and it is capable to promote GBM cell proliferation and growth. Mechanistically, LINC01426 serves as a molecular sponge to sequester the miR345-3p and thus enhancing the level of VAMP8, an oncogenic coding gene, to promote GBM progression. Conclusions:Our results revealed the detailed mechanisms of LINC01426 facilitated cell proliferation and growth in GBM and report the clinical value of LINC01426 for GBM prognosis and treatment.

SUBMITTER: Cao J

PROVIDER: S-EPMC7372762 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Long non-coding RNA LINC01426 facilitates glioblastoma progression via sponging miR-345-3p and upregulation of VAMP8.

Cao Jingwei J Tang Zhanbin Z Su Zhiqiang Z

Cancer cell international 20200720

<h4>Background</h4>Long non-coding RNAs (lncRNAs) has been extensively reported play important roles in regulating the development and progression of cancers, including Glioblastoma (GBM). LINC01426 is a novel lncRNA that has been identified as an oncogenic gene in GBM. Herein, we attempted to elucidate the detailed functions and underlying mechanisms of LINC01426 in GBM.<h4>Methods</h4>LINC01426 expression in GBM cell lines and tissues were detected by quantitative real-time PCR (qRT-PCR). Cell ...[more]

PMID: 32699526

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Project description:BackgroundLong noncoding RNAs (lncRNAs) have been reported to play a key role in the development and progression of human malignancies. FLJ33360 is an lncRNA with unknown functions. This study was designed to determine the clinical significance and mechanism of FLJ33360 in ovarian cancer.Materials and methodsThe clinical significance of FLJ33360 in ovarian cancer was determined using the Gene Expression Profiling Interactive Analysis (GEPIA) database, Kaplan-Meier Plotter database, quantitative reverse transcription polymerase chain reaction (qRT-PCR) and statistical analysis. The regulatory relationships between FLJ33360 and miR-30b-3p were explored through bioinformatics, the Gene Expression Omnibus (GEO) database, the ArrayExpress database and meta-analysis. The possible pathways were predicted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. In addition, the key target genes were identified using a protein-protein interaction (PPI) network, the Cancer Genome Atlas (TCGA) database, and correlation analysis.ResultsFLJ33360 expression was significantly downregulated in ovarian cancer tissue (P=0.0011) and was closely associated with International Federation of Gynecology and Obstetrics (FIGO) stage (P=0.027) and recurrence (P=0.002). FLJ33360 may have potential value in detecting ovarian cancer (area under the curve =0.793). Function analysis demonstrated that FLJ33360 can act as a molecular sponge of miR-30b-3p to regulate the expression of target genes that are mainly involved in positive regulation of smooth muscle cell migration, the unsaturated fatty acid metabolic process, and positive regulation of the epithelial to mesenchymal transition. Among these target genes, BCL2 is the hub gene.ConclusionFLJ33360 is a potential biomarker for early diagnosis and prognostic assessment in ovarian cancer and may regulate the expression of genes by sponging miR-30b-3p and thus participate in the development of ovarian cancer.

Project description:BackgroundGEFT is a key regulator of tumorigenesis in rhabdomyosarcoma (RMS), and overexpression of GEFT is significantly correlated with distant metastasis, lymph node metastasis, and a poor prognosis, yet the underlying molecular mechanism is still poorly understood. This study aimed to investigate and validate the molecular mechanism of GEFT-activated lncRNAs in regulating mTOR expression to promote the progression of RMS.MethodsGEFT-regulated lncRNAs were identified through microarray analysis. The effects of GEFT-regulated lncRNAs on the proliferation, apoptosis, invasion, and migration of RMS cells were confirmed through cell functional experiments. The target miRNAs of GEFT-activated lncRNAs in the regulation of mTOR expression were predicted by bioinformatics analysis combined with quantitative real-time polymerase chain reaction (qRT-PCR) analysis. The expression of lnc-PSMA8-1, miR-144-3p, and mTOR was measured by qRT-PCR in RMS tissue samples and cell lines. The regulatory mechanisms of the lnc-PSMA8-1-miR-144-3p-mTOR signaling axis were verified by RNA-binding protein immunoprecipitation (RIP), a luciferase reporter assay, qRT-PCR analysis, Western blot analysis, and cell functional experiments.ResultsThe microarray-based analysis identified 31 differentially expressed lncRNAs (fold change > 2.0, P < 0.05). Silencing the 4 upregulated lncRNAs (lnc-CEACAM19-1, lnc-VWCE-2, lnc-GPX7-1, and lnc-PSMA8-1) and overexpressing the downregulated lnc-FAM59A-1 inhibited the proliferation, invasion, and migration and induced the apoptosis of RMS cells. Among the factors analyzed, the expression of lnc-PSMA8-1, miR-144-3p, and mTOR in RMS tissue samples and cells was consistent with the correlations among their expression indicated by the lncRNA-miRNA-mRNA regulatory network based on the ceRNA hypothesis. lnc-PSMA8-1 promoted RMS progression by competitively binding to miR-144-3p to regulate mTOR expression.ConclusionOur research demonstrated that lnc-PSMA8-1 was activated by GEFT and that the former positively regulated mTOR expression by sponging miR-144-3p to promote the progression of RMS. Therefore, targeting this network may constitute a potential therapeutic approach for the management of RMS.

Dataset Information

Long non-coding RNA LINC01426 facilitates glioblastoma progression via sponging miR-345-3p and upregulation of VAMP8.

Publications

Long non-coding RNA LINC01426 facilitates glioblastoma progression via sponging miR-345-3p and upregulation of VAMP8.

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