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Research Paper|Volume 12, Issue 3|pp 2156—2168

Knockdown of P3H4 inhibits proliferation and invasion of bladder cancer

Lin Hao1,2, Kun Pang1,2, Hui Pang3, Junjie Zhang1, Zhiguo Zhang1,2, Houguang He1,4, Rongsheng Zhou1, Zhenduo Shi1, Conghui Han1,2
  • 1Department of Urology, Xuzhou Central Hospital, Xuzhou 221009, Jiangsu, China
  • 2The Third Affiliated Hospital of Soochow University, Changzhou 213000, Jiangsu, China
  • 3Central Laboratory, Xuzhou Central Hospital, Xuzhou 221009, Jiangsu, China
  • 4College of Science and Technology, Jiangsu Normal University, Xuzhou 221009, Jiangsu, China
* Equal contribution and co-first authors
Received: November 2, 2019Accepted: January 2, 2020Published: February 4, 2020
https://doi.org/10.18632/aging.102732

Copyright: © 2020 Hao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The prolyl 3-hydroxylase family member 4 (P3H4) (alias SC65) is implicated in a variety of physiological and pathological processes. However, little is known about the role of P3H4 in tumors. This study aimed to investigate the role of P3H4 in bladder cancer (BC) and the regulatory mechanisms that influence its expression. P3H4 was highly expressed in BC tissues. Knockdown of P3H4 inhibited BC cell proliferation, cell cycle, migration and invasion in vitro, and inhibited BC growth in vivo. We also found that ETV4 bound directly to the promoter region of P3H4 and activated its transcription. Furthermore, overexpression of ETV4 rescued the inhibition of proliferation and invasion induced by PH4 silencing. ETV4 was significantly overexpressed in the BC tissues. In conclusion, P3H4 functioned an oncogene role in BC progression, and ETV4 bound directly to the P3H4 promoter region to regulate its transcription.