EZH2型
PRC2
癌症研究
前列腺癌
甲基转移酶
癌变
蛋白激酶B
生物
组蛋白H3
转录因子
组蛋白甲基转移酶
细胞周期检查点
表观遗传学
基因敲除
细胞生长
组蛋白
甲基化
细胞周期
心理压抑
信号转导
细胞生物学
癌症
细胞培养
基因表达
遗传学
基因
作者
John Pedersen,Tao Wang,Kang‐Jing Li,Ling-Hong Hu,Yue Li,Yu‐Zhong Yu,Tao Xie,Sha Zhu,Du-Jiang Fu,Li Wang,Hong-Peng Fang,Fengping Liu,Hong Chen,Zhe‐Sheng Chen,Ninghan Feng,Jinghua Liu,Yong Jiang,John Pedersen
出处
期刊:Cancer Letters
[Elsevier]
日期:2023-10-24
卷期号:579: 216464-216464
被引量:1
标识
DOI:10.1016/j.canlet.2023.216464
摘要
The suppressor of variegation enhancer of zeste-trithorax (SET) domain methyltransferases have been reported to function as key regulators in multiple tumor types by catalyzing histone lysine methylation. Nevertheless, our understanding on the role of these lysine methyltransferases, including SETD4, in prostate cancer (PCa) remains limited. Hence, the specific role of SETD4 in PCa was investigated in this study. The expression of SETD4 in PCa cells and tissue samples was downregulated in PCa cells and tissue specimens, and decreased SETD4 expression led to inferior clinicopathological characteristics in patients with PCa. knockdown of SETD4 facilitated the proliferation of PCa cells and accelerated cell cycle progression. Mechanistically, SETD4 repressed NUPR1 transcription by methylating H3K27 to generate H3K27me3, subsequently inactivated Akt pathway and impeded the tumorigenesis of PCa. Our results highlight that SETD4 prevents the development of PCa by catalyzing the methylation of H3K27 and suppressing NUPR1 transcription, subsequently inactivating the Akt signaling pathway. The findings suggest the potential application of SETD4 in PCa prognosis and therapeutics.
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