Long non-coding RNA CHRF promotes proliferation and mesenchymal transition (EMT) in prostate cancer cell line PC3 requiring up-regulating microRNA-10b.

Abstract

Despite the advance of diagnosis and treatment for prostate cancer, the prognosis of metastatic prostate cancer is poor. We aimed to explore the functional role of long non-coding RNA cardiac hypertrophy-related factor (lncRNA CHRF) in prostate cancer cells (PC3) as well as the molecular mechanisms. LncRNA CHRF silence repressed cell number (%), down-regulated expression of cyclinD1, CDK4 and CDK6, and promoted apoptosis along with activation of the casapse-3 and caspase-9. LncRNA CHRF promoted mesenchymal transition (EMT), showing down-regulation of E-cadherin and up-regulation of N-cadherin, vimentin and ZEB1. Afterwards, we found miR-10b expression was positively correlated with lncRNA CHRF expression, and miR-10b inhibition could reverse the effects of lncRNA CHRF on PC3 and LNCaP cell proliferation and EMT. Finally, lncRNA CHRF was found to activate the GSK3β/AKT and NF-κB pathways via up-regulation of miR-10b. LncRNA CHRF silence repressed proliferation and EMT while promoted apoptosis in PC3 cells via positive regulation of miR-10b. The GSK3β/AKT and NF-κB pathways were activated by lncRNA CHRF, possibly through up-regulation of miR-10b.