Open Access
Cell Reports, volume 43, issue 7, pages 114431
Elevating PLK1 overcomes BETi resistance in prostate cancer via triggering BRD4 phosphorylation-dependent degradation in mitosis
Yanquan Zhang
1, 2
,
Ka Wing Fong
1, 2
,
Fengyi Mao
1
,
Ruixin Wang
1
,
Derek B. Allison
3
,
Dana Napier
4
,
Daheng He
2, 5
,
Jinpeng Liu
2, 5
,
Zhijun Zhang
6
,
Jing Chen
7
,
Yifan Kong
1
,
Chaohao Li
1
,
Guangbing Li
8
,
Jinghui Liu
1, 2
,
Zhi Guo Li
1, 2
,
HAINING ZHU
7
,
Chi Wang
2, 5
,
Xiaoqi Liu
1, 2
6
7
Publication type: Journal Article
Publication date: 2024-07-04
Journal:
Cell Reports
scimago Q1
wos Q1
SJR: 4.279
CiteScore: 13.8
Impact factor: 7.5
ISSN: 22111247, 26391856
Abstract
Bromodomain-containing protein 4 (BRD4) has emerged as a promising therapeutic target in prostate cancer (PCa). Understanding the mechanisms of BRD4 stability could enhance the clinical response to BRD4-targeted therapy. In this study, we report that BRD4 protein levels are significantly decreased during mitosis in a PLK1-dependent manner. Mechanistically, we show that BRD4 is primarily phosphorylated at T1186 by the CDK1/cyclin B complex, recruiting PLK1 to phosphorylate BRD4 at S24/S1100, which are recognized by the APC/C
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