Transcription Factor ETS1 Promotes Glioma Cell Growth by Activating LncRNA XIST
10.3971/j.issn.1000-8578.2024.23.1055
- VernacularTitle:转录因子ETS1激活长链非编码RNA XIST促进胶质瘤细胞增殖
- Author:
Ran LUO
1
;
Wenyi LUO
;
Mingkai LU
;
Meng ZHOU
;
Yanting LIU
;
Chunlei TIAN
Author Information
1. Neurosurgery of The First College of Clinical Medical Science, China Three Gorges University and Yichang Central People’s Hospital, Yichang 443003, China
- Publication Type:Research Article
- Keywords:
Glioma;
ETS1;
LncRNA XIST
- From:
Cancer Research on Prevention and Treatment
2024;51(5):328-335
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the biological function and downstream mechanism of ETS1 in glioma. Methods Bioinformatics and immunohistochemistry were used to analyze the differential expression characteristics of ETS1 in gliomas; qRT-PCR was employed to detect the expression level of ETS1 mRNA and lncRNA X-inactive specific transcript (XIST). CCK-8 and 5-ethyl-2′-deoxyuridine experiments were conducted to detect cell growth. Western blot was used to detect the expression of apoptosis-related proteins (Bax, Bak, Bcl-2). PROMO database was utilized to predict the binding sites between ETS1 and XIST promoter. Dual-luciferase reporter gene assay and chromatin immunoprecipitation-quantitative polymerase chain reaction assays were performed to verify the binding relationship between ETS1 and the XIST promoter region. cBioPortal database was used to analyze the correlation between the expression of ETS1 mRNA and XIST in glioma tissues. Results The expression levels of ETS1 mRNA and protein were significantly upregulated in glioma (P<0.05). The depletion of ETS1 significantly inhibited the proliferation of glioma cells and promoted cell apoptosis (P<0.05). ETS1 could target and bind with the XIST promoter and promote the expression of XIST (P<0.05). The overexpression of XIST reversed the effects of ETS1 on the proliferation of glioma cells and the promotion of cell apoptosis (P<0.05). Conclusion ETS1 is highly expressed in glioma tissues. It could promote the expression of lncRNA XIST, boost the proliferation of glioma cells, and inhibit cell apoptosis.
