SCARNA10 regulates p53 acetylation-dependent transcriptional activity

被引:4
作者
Wu, Yanxia [1 ]
Sun, Yanxi [1 ]
Xu, Binchu [1 ]
Yang, Mo [1 ]
Wang, Xingwu [1 ]
Zhao, Xiaocheng [1 ]
机构
[1] Sun Yat Sen Univ, Affiliated Hosp 7, Mol Canc Res Ctr, Sch Med, Shenzhen 518107, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
SCARNA10; p53; Transcription; LONG NONCODING RNA; CELL-CYCLE ARREST; DNA-BINDING; ACTIVATION; APOPTOSIS; REVEALS;
D O I
10.1016/j.bbrc.2023.05.091
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The tumor suppressor p53 is involved in variety of cell progresses including cell cycle arrest, apoptosis, DNA repair, senescence, cell metabolism and ferroptosis. Here, we identified lncRNA SCARNA10 (Small Cajal Body-Specific RNA 10) as a novel cellular factor that interacts with the DNA binding domain (DBD) of p53. Upon binding the DBD of p53 and CREB-binding protein (CBP), SCARNA10 promotes the acety-lation of p53, and activates p53-mediated transcriptional activation. Overexpress or knockdown SCARNA10 leads to up (or down)-regulation of p53-mediated transcriptional activation, whereas not affecting p53 protein levels. Moreover, SCARNA10 directly activates transcription by increasing the acetylation of p53 C-terminal domain (CTD) without affecting p53 phosphorylation at Ser15. These re-sults indicate that SCARNA10 is a novel factor which regulates p53 acetylation-dependent transcriptional activity and tumor suppression. & COPY; 2023 Elsevier Inc. All rights reserved.
引用
收藏
页码:38 / 45
页数:8
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