癌症研究
HDAC1型
转录因子
髓系白血病
YY1年
细胞生物学
相扑蛋白
生物
化学
发起人
基因表达
基因
组蛋白
遗传学
泛素
组蛋白脱乙酰基酶
作者
Meng Li,Mingying Li,Tao Sun,Chunyan Ji
出处
期刊:Blood
[American Society of Hematology]
日期:2022-11-15
卷期号:140 (Supplement 1): 11485-11485
被引量:1
标识
DOI:10.1182/blood-2022-168417
摘要
Methyltransferase-like protein 3 (METTL3) plays critical roles in acute myeloid leukemia (AML) progression, however, the mechanism of abnormal overexpression of METTL3 in AML remain elusive. In the current study, we uncovered that Yin Yang 1 (YY1) binds to the promoter region of METTL3 as a transcription factor and promotes its expression, which in turn enhances the proliferation of AML cells. Mechanistically, YY1 binds to HDAC1/3 and regulates METTL3 expression in a moderate liquid-liquid phase separation (LLPS) manner. After mutation of the HDAC-binding site of YY1 or HDAC inhibitor (HDACi) treatment, YY1 was separated from HDAC1/3, which resulted in an excessive LLPS state, thereby inhibiting the expression of METTL3 and the proliferation of AML cells. In conclusion, our study clarified the regulatory mechanism of the abnormal expression of METTL3 in AML, revealed the precise "Yin-Yang" regulatory mechanism of YY1 from the perspective of LLPS degree, and provided new ideas for the precise diagnosis and treatment of AML.
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