MIR663AHG as a competitive endogenous RNA regulating TGF‐β‐induced epithelial proliferation and epithelial–mesenchymal transition in benign prostate hyperplasia

Author:

Tong Shiyu1ORCID,Mo Miao1,Hu Xiheng1,Wu Longxiang1,Chen Minfeng1,Zhao Cheng1

Affiliation:

1. Department of Urology Surgery Xiangya Hospital of Central South University Changsha P.R. China

Abstract

AbstractBenign prostate hyperplasia (BPH) is the most commonly seen disease among aging males. Transforming growth factor(TGF)‐β‐mediated epithelial–mesenchymal transition (EMT) and epithelial overproliferation might be central events in BPH etiology and pathophysiology. In the present study, long noncoding RNA MIR663AHG, miR‐765, and FOXK1 formed a competing endogenous RNAs network, modulating TGF‐β‐mediated EMT and epithelial overproliferation in BPH‐1 cells. miR‐765 expression was downregulated in TGF‐β‐stimulated BPH‐1 cells; miR‐765 overexpression ameliorated TGF‐β‐mediated EMT and epithelial overproliferation in BPH‐1 cells. MIR663AHG directly targeted miR‐765 and negatively regulated miR‐765; MIR663AHG knockdown also attenuated TGF‐β‐induced EMT and epithelial overproliferation in BPH‐1 cells, whereas miR‐765 inhibition attenuated MIR663AHG knockdown effects on TGF‐β‐stimulated BPH‐1 cells. miR‐765 directly targeted FOXK1 and negatively regulated FOXK1. FOXK1 knockdown attenuated TGF‐β‐induced EMT and epithelial overproliferation and promoted autophagy in BPH‐1 cells, and partially attenuated miR‐765 inhibition effects on TGF‐β‐stimulated BPH‐1 cells. In conclusion, this study provides a MIR663AHG/miR‐765/FOXK1 axis modulating TGF‐β‐induced epithelial proliferation and EMT, which might exert an underlying effect on BPH development and act as therapeutic targets for BPH treatment regimens.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Toxicology,Molecular Biology,Molecular Medicine,Biochemistry,General Medicine

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