Mechanism of SOS1-IT1 promoting EZH2 expression in human endometrial cancer cells by regulating acetylation modification
10.16098/j.issn.0529-1356.2025.04.009
- VernacularTitle:SOS1-IT1通过调控乙酰化修饰促进人子宫内膜癌细胞EZH2表达的机制
- Author:
Hong-Yang LIU
1
;
Xue-Ling LOU
;
Rong-Jing ZHANG
;
Quan-Ling FENG
;
Kai-Ge GUO
;
Hao-Fan WANG
;
Ying-Ying LI
;
Jun-Hu WAN
;
Lin-Dong ZHANG
Author Information
1. 郑州大学第三附属医院妇科
- Keywords:
Endometrial cancer;
Long non-coding RNA;
SOS Ras/Rac guanine nucleotide exchange factor 1-intronic transcript 1;
Enhancer of zeste homolog 2;
Western blotting;
Human
- From:
Acta Anatomica Sinica
2025;56(4):444-451
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the molecular mechanism by which SOS Ras/Rac guanine nucleotide exchange factor 1-intronic transcript 1(SOS1-IT1)affects enhancer of zeste homolog 2(EZH2)protein expression in endometrial cancer cells Ishikawa and RL95-2.Methods Lentiviral transfection of short hairpin RNA(shRNA)and overexpression plasmid were used in Ishikawa and RL95-2 cell lines to knock down and overexpress SOS1-IT1.The mechanism of EZH2 expression regulation was studied using Real-time PCR,Western blotting,and chromatin immunoprecipitation.Results The expression of SOS1-IT1 and EZH2 genes was positively correlated in endometrial cancer tissues.Knocking down SOS1-IT1 significantly reduces the expression of EZH2,inhibited the proliferation and migration of Ishikawa and RL95-2 cells,and could reduced the acetylation of histone H3 at position 27(H3K27)and the enrichment of CREB binding protein(CBP)in the EZH2 gene promoter region.Overexpression of SOS1-IT1 could increased the expression of EZH2 and enhance the acetylation of H3K27 and the enrichment of CBP.CBP could bind to SOS1-IT1 RNA,and this binding ability was weakened when CBP was knocked down.Conclusion SOS1-IT1 can promote the expression level of EZH2 in endometrial cancer cells Ishikawa and RL95-2 by regulating the acetylation modification level of the EZH2 gene promoter region,thereby affecting the proliferation and migration ability of endometrial cancer cells.
