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Long non-coding RNA MAGI2-AS3 inactivates STAT3 pathway to inhibit prostate cancer cell proliferation via acting as a microRNA-424-5p sponge.

ABSTRACT: Aberrant expression of long non-coding RNAs (lncRNAs) that results in sustained activation of cell growth promoting pathways is an important mechanism in driving prostate cancer progression. In the present study, we explored differentially expressed lncRNAs in two microarray datasets of prostate benign and malignant tissues. We found that MAGI2-AS3 was one of the most downregulated lncRNAs in prostate tumors, which was further confirmed in our collected clinical samples. The function assays showed that MAGI2-AS3 overexpression decreased cell viability and led to obvious cell apoptosis in PC-3 and DU145 prostate cancer cells. Elevation of MAGI2-AS3 decreased the activity of STAT3 in PC-3 and DU145. In addition, microRNA-424-5p (miR-424-5p), a positive regulator of STAT3 pathway, was predicted as a target of MAGI2-AS3, furthermore, the interaction between MAGI2-AS3 and miR-424-5p was confirmed via reverse-transcript polymerase chain reaction (RT-qPCR), dual luciferase reporter assay and RNA immunoprecipitation (RIP). MAGI2-AS3 upregulated miR-424-5p and downregulated COP1 in PC-3 and DU145. More importantly, IL6-induced activation of STAT3 pathway could attenuate the biological effect of MAGI2-AS3 in PC-3 and DU145. In clinical samples, MAGI2-AS3 levels were negatively correlated with miR-424-5p expression, while positively correlated with COP1 mRNA expression. Altogether, the current study revealed MAGI2-AS3 as a novel negative regulator of prostate cancer development.

SUBMITTER: Wei X

PROVIDER: S-EPMC8692692 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundLung cancer is a malignant tumor that seriously threatens the health of human beings. Long non-coding RNAs (lncRNAs) are thought to play important roles in the pathophysiology of lung cancer. In this study, we identified a new lncRNA, MAGI2-AS3 in non-small cell lung cancer (NSCLC) tissues by conducting an integrated bioinformatics analysis. Mechanistic studies were also performed to explore the biological functions of MAGI2-AS3 in NSCLC progression.MethodsA bioinformatics analysis was conducted to determine the prognostic role of MAGI2-AS3. CCK-8, EdU assay, colony formation and Transwell were performed to determine the effects of MAGI2-AS3 on the progression of NSCLC cells. A nude mice model was used to evaluate the effects of MAGI2-AS2 on the in vivo tumor growth of NSCLC. Luciferase reporter and RNA pull-down assays were used to evaluate interactions between MAGI2-AS3 and its downstream targets.ResultsMAGI2-AS3 was found to be downregulated in NSCLC tissues. The gain-of-function in vitro studies showed that the overexpression of MAGI2-AS3 suppressed NSCLC cell proliferation and invasion. Conversely, the knockdown of MAGI2-AS3 had the opposite effects. The bioinformatics analysis and luciferase report assay revealed that MAGI2-AS3 functioned as competing endogenous RNA to suppress microRNA (miR)-629-5p expression, while miR-629-5p suppressed thioredoxin-interacting protein (TXNIP) expression by targeting its 3' untranslated region. The rescue experiment results showed that MAGI2-AS3 knockdown enhanced NSCLC cell progression (increasing cell proliferation and invasion, but reducing cell apoptosis), which was counteracted by miR-629-5p inhibition or TXNIP overexpression.ConclusionsThe study revealed that MAGI2-AS3 was downregulated in NSCLC tissues and cells, and MAGI2-AS3 suppressed NSCLC cell progression. Further, the mechanistic results showed that MAGI2-AS3 exerted a tumor-suppressive effect in NSCLC by targeting the miR-629-5p/TXNIP axis.

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Long non-coding RNA MAGI2-AS3 inactivates STAT3 pathway to inhibit prostate cancer cell proliferation via acting as a microRNA-424-5p sponge.

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