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Updated: Dec 29, 2025

3-D Cell Culture System for Studying Invasion and Evaluating Therapeutics in Bladder Cancer
Published on: September 13, 2018
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.
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.
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.
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