Knockdown of P3H4 inhibits proliferation and invasion of bladder cancer

Lin Hao1,2, Kun Pang1,2, Hui Pang3

  • 1Department of Urology, Xuzhou Central Hospital, Xuzhou 221009, Jiangsu, China.

Aging
|February 5, 2020
PubMed

Insights

Prolyl 3-hydroxylase family member 4 (P3H4) acts as an oncogene in bladder cancer (BC). Its expression is upregulated by ETV4, promoting BC cell proliferation and invasion.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Prolyl 3-hydroxylase family member 4 (P3H4), also known as SC65, is involved in various biological processes.
  • The specific role of P3H4 in tumor development, particularly in bladder cancer (BC), remains largely unexplored.

Purpose of the Study:

  • To investigate the function of P3H4 in bladder cancer progression.
  • To elucidate the regulatory mechanisms controlling P3H4 expression in BC.

Main Methods:

  • Analysis of P3H4 expression in BC tissues.
  • In vitro and in vivo experiments involving P3H4 knockdown in BC cells.
  • Chromatin immunoprecipitation (ChIP) assays to assess ETV4 binding to the P3H4 promoter.
  • Overexpression studies of ETV4 in BC cells.

Main Results:

  • P3H4 was found to be highly expressed in bladder cancer tissues.
  • Silencing P3H4 significantly inhibited BC cell proliferation, cell cycle progression, migration, and invasion in vitro, and suppressed tumor growth in vivo.
  • ETV4 directly binds to the promoter region of P3H4, activating its transcription.
  • Overexpression of ETV4 counteracted the inhibitory effects of P3H4 knockdown on BC cell proliferation and invasion.
  • ETV4 was significantly overexpressed in BC tissues.

Conclusions:

  • P3H4 plays a crucial oncogenic role in the progression of bladder cancer.
  • ETV4 directly regulates P3H4 transcription by binding to its promoter, contributing to bladder cancer development.