GATA3 mediates the effect of miR-21/PTEN axis on the proliferation and invasion of endometrial cancer cells
10.3969/j.issn.1006-5725.2024.15.005
- VernacularTitle:GATA3介导miR-21/PTEN轴对子宫内膜癌细胞增殖、侵袭的影响
- Author:
Fahui WANG
1
;
Qingchun DENG
;
Jiajia LIN
;
Chunfei CHEN
Author Information
1. 海南医学院第二附属医院妇科(海口 570311)
- Keywords:
endometrial carcinoma;
GATA binding protein 3;
microRNA-21;
phosphatase and tensin homologues of human chromosome 10 deletion;
proliferate;
invasion
- From:
The Journal of Practical Medicine
2024;40(15):2069-2074
- CountryChina
- Language:Chinese
-
Abstract:
Objective To analyze the effects of GATA binding protein 3(GATA3)mediated mini RNA-21(miR-21)/phosphatase and tensin homologue(PTEN)axis missing from human chromosome Chromosome 10 on the proliferation and invasion of endometrial cancer cells.Methods HEC-1-A cells were transfected and divided into control group,GATA3 empty plasmid group,GATA3 overexpression plasmid group,GATA3 siRNA negative control group,and GATA3 siRNA group.Detect the expression levels of GATA3,miR-21,PTEN,proliferation,apoptosis rate,migration,and invasion in each group of cells.Results Compared with the hEEC group,the expression levels of GATA3 and miR-21 in cells of the HEC-1-A group,HEC-1-B group,and Ishikawa group increased,while the expression levels of PTEN decreased(P<0.05).Compared with the GATA3 empty plasmid group,the GATA3 overexpression plasmid group showed an increase in GATA3,miR-21 mRNA expression,pro-liferation rate,migration distance,number of invading cells,and Vimentin levels,while the PTEN mRNA expression,apoptosis rate,Caspase-9,Bax,and E-cadherin levels decreased(P<0.05);Compared with the GATA3 siRNA negative control group,the GATA3,miR-21 mRNA expression,proliferation rate,migration distance,number of invading cells,and Vimentin level decreased,while the PTEN mRNA expression,apoptosis rate,Caspase-9,Bax,and E-cadherin levels increased(P<0.05).Conclusion Downregulation of GATA3 expression can regulate the miR-21/PTEN axis,slow down the proliferation of HEC-1-A cells,and promote apoptosis of HEC-1-A cells.
