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Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-β1/ Smad signaling pathway.

Research paper by Bin B Zhao, Yong Y Yang, Li-Bing LB Hu, Yu Y Bai, Rui-Qian RQ Li, Guo-Yin GY Zhang, Jun J Li, Cheng-Wei CW Bi, Li-Bo LB Yang, Chen C Hu, Yong-Hong YH Lei, Qi-Lin QL Wang, Zhi-Min ZM Liu, Yu-Lin YL Lu

Indexed on: 28 Dec '17Published on: 28 Dec '17Published in: Cancer biomarkers : section A of Disease markers



Abstract

Long non-coding RNAs (lncRNAs) were playing critical roles in tumorigenesis. However, in prostate cancer, the roles and mechanisms of lncRNAs especially ANRIL were largely unknown. We investigated the effects of ANRIL on the proliferation and migration of prostate cancer cells using CCK-8 assay and Transwell migration assay. Real-time PCR and western blotting assays were used to analyze the levels of ANRIL, let-7a, TGF-β1, p-Smad2 and p-Smad7. Our results showed that ANRIL was significantly overexpressed in prostate cancer tissues compared with corresponding normal tissues. Knockdown of ANRIL significantly inhibited the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells. Knockdown of ANRIL significantly decreased the levels of TGF-β1 and p-Smad2, and increased the level of p-Smad7 in prostate cancer LNCap cells. We further found that knockdown of ANRIL significantly enhanced the expression of let-7a, and rescue experiment found that let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the proliferation and migration of prostate cancer LNCap, PC3 and DU145 cells. And let-7a inhibitor recovered the suppressive effects of ANRIL silencing on the activity of TGF-β1/Smad signaling pathway in prostate cancer LNCap cells. Taken together, our findings indicated that overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-β1/Smad signaling pathway.