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

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 ben...

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Veröffentlicht in:Journal of Cancer 2022, Vol.13 (1), p.343-353
Hauptverfasser: Wei, Xin, Hou, Yi, Zhang, Yan, Zhang, Huaiwei, Sun, Zhou, Meng, Xiangdi, Wang, Zhixin
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Sprache:eng
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Zusammenfassung: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 was one of the most downregulated lncRNAs in prostate tumors, which was further confirmed in our collected clinical samples. The function assays showed that overexpression decreased cell viability and led to obvious cell apoptosis in PC-3 and DU145 prostate cancer cells. Elevation of 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 , furthermore, the interaction between and miR-424-5p was confirmed via reverse-transcript polymerase chain reaction (RT-qPCR), dual luciferase reporter assay and RNA immunoprecipitation (RIP). 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 in PC-3 and DU145. In clinical samples, levels were negatively correlated with miR-424-5p expression, while positively correlated with mRNA expression. Altogether, the current study revealed as a novel negative regulator of prostate cancer development.
ISSN:1837-9664
1837-9664
DOI:10.7150/jca.60749