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Volume 25, Issue 2 (March 2023) 25, 152–157; 10.4103/aja202287

CHD1 deletion stabilizes HIF1α to promote angiogenesis and glycolysis in prostate cancer

Wang, Yu-Zhao1; Qian, Yu-Chen1; Yang, Wen-Jie1; Ye, Lei-Hong1; Guo, Guo-Dong1; Lv, Wei1; Huan, Meng-Xi1; Feng, Xiao-Yu1; Wang, Ke1; Yang, Zhao1,2; Gao, Yang1,2; Li, Lei1,2,; Chen, Yu-Le1,2,

1Department of Urology, the First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, China

2Oncology Research Laboratory, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi’an 710061, China

Correspondence: Dr. L Li (lilydr@163.com) or Dr. YL Chen (cylxdwyd@126.com)

Received: 15 June 2022; Accepted: 02 November 2022; published online: 10 January 2023


Chromodomain-helicase-DNA-binding protein 1 (CHD1) deletion is among the most common mutations in prostate cancer (PCa), but its role remains unclear. In this study, RNA sequencing was conducted in PCa cells after clustered regularly interspaced palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9)-based CHD1 knockout. Gene set enrichment analysis (GSEA) indicated upregulation of hypoxia-related pathways. A subsequent study confirmed that CHD1 deletion significantly upregulated hypoxia-inducible factor 1α (HIF1α) expression. Mechanistic investigation revealed that CHD1 deletion upregulated HIF1α by transcriptionally downregulating prolyl hydroxylase domain protein 2 (PHD2), a prolyl hydroxylase catalyzing the hydroxylation of HIF1α and thus promoting its degradation by the E3 ligase von Hippel–Lindau tumor suppressor (VHL). Functional analysis showed that CHD1 deletion promoted angiogenesis and glycolysis, possibly through HIF1α target genes. Taken together, these findings indicate that CHD1 deletion enhances HIF1α expression through PHD2 downregulation and therefore promotes angiogenesis and metabolic reprogramming in PCa.

Keywords: angiogenesis; CHD1; HIF1α; metabolism; prostate cancer

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Asian Journal of Andrology CN 31-1795/R ISSN 1008-682X  Copyright © 2023  Shanghai Materia Medica, Chinese Academy of Sciences.  All rights reserved.