乙酰化
生物
转录因子
磷酸化
赖氨酸
癌症研究
细胞生物学
癌变
癌症
组蛋白
生物化学
遗传学
基因
氨基酸
作者
Yan Liu,Yuan-Yue Zhang,Xiaogang Wang,Min Li,Yuehong Long,Yufeng Li,Yan-Kun Liu,Yuhui Li,Yaqi Wang,Jiang-Sheng Mi,Cheng-Hua Yu,Deyan Li,Jinghua Zhang,Xiaojun Zhang
出处
期刊:Oncogene
[Springer Nature]
日期:2020-06-09
卷期号:39 (27): 5056-5067
被引量:10
标识
DOI:10.1038/s41388-020-1350-0
摘要
Williams syndrome transcription factor (WSTF) is a transcription factor and tyrosine kinase. WSTF overexpression promotes migration and proliferation of various cancers, and Ser158 (WSTFS158) phosphorylation plays an important role in this process. However, the role of the other posttranslational modifications of WSTF is unknown. Here, we report that lysine (K) 426 on WSTF is acetylated by MOF and deacetylated by SIRT1. Mechanistically, male-specific lethal (MSL) 1v1 interaction with WSTF facilitates its interaction with MOF for WSTF acetylation, which in turn promotes WSTFS158 phosphorylation. The kinase and transcriptional regulatory activity of WSTF were enhanced by acetylation. WSTFK426ac levels positively and significantly correlated with tumor size, histological grade, and age. Moreover, we demonstrated that acetylated WSTF promotes cancer cell proliferation, migration, invasion, and tumor formation. In conclusion, we identified the enzymes regulating WSTF K426 acetylation, and demonstrated an acetylation-dependent mechanism that modulates the activities of WSTF and contributes to tumorigenesis. Our findings provide new clues to study WSTF-mediated normal development and disease.
科研通智能强力驱动
Strongly Powered by AbleSci AI