miR-200a involvement in the biological behavior of hepatoma carcinoma cells by targeting the regulatory expression of mesenchymal-epithelial transition factor
10.3760/cma.j.cn501113-20231108-00184
- VernacularTitle:miR-200a靶向调控间质表皮转化因子的表达参与肝癌细胞生物学行为
- Author:
Liang ZHANG
1
;
Wei CHEN
;
Zhenguo HOU
;
Xi YANG
;
Minghui LIU
Author Information
1. 邢台市人民医院放射科，邢台 054000
- Keywords:
Liver cancer;
miR-200a;
Mesenchymal epidermal transforming factor;
Hepatoma cells;
Biological behavior;
Apoptosis
- From:
Chinese Journal of Hepatology
2023;31(11):1176-1181
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the regulatory effect of miR-200a on mesenchymal-epithelial transition factor (MET) and its impact on the biological behavior of hepatoma carcinoma cells.Method:A luciferase reporter assay was used to determine miR-200a's regulatory impact on MET. Human hepatoma HepG2 cells were divided into a control group, a miR-200a group, a MET overexpression group, and a co-transfection group (miR-200a+MET). After culture, cell proliferation ability, cell migration ability, apoptosis, cell invasion ability, and the expression of MET and apoptosis-related (Bcl-2, Caspase-3, Bax) proteins were detected and observed by cell counting kit-8 (CCK-8), scratch assay, Annexin V-FITC staining, transwell chambers, and western blotting. The two groups were compared using the independent sample t-test. The multiple groups were statistically analyzed using one-way ANOVA.Results:The luciferase experiment showed that miR-200a had target MET. The proliferation rate, number of invasions in cells (55.00 ± 7.21, 85.00 ± 7.94, 164.67 ± 19.22, 104.00± 12.29), scratch healing rate (28.33% ± 5.03%, 61.67% ± 4.04%, 74.67% ± 7.02%, 49.33% ± 9.02%), and expression levels of MET, Bcl-2, and Caspase-3 proteins were lower in the miR-200a group than those in the control group, MET overexpression group, and co-transfection group, while the MET overexpression group had higher indexes than the other three groups, with statistically significant differences between the groups ( P <0.05). The apoptosis rate of HepG2 cells and the expression level of Bax protein were higher in the miR-200a group than those in the control group, MET overexpression group, and co-transfection group (19.25% ± 2.98%, 6.80% ± 1.15%, 3.42% ±0.76%, 9.90% ± 2.72%), while the levels of various indexes in the MIF overexpression group were lower than those in the other three groups. The control group and co-transfection group were between the two groups, and the difference between the groups was statistically significant ( P <0.05). Conclusion:HepG2 cell proliferation, migration, invasion, and cell apoptosis induction can be inhibited by miR-200a, and the functional mechanism for this may be associated with the miR-200a target’s ability to down-regulate MET expression in HepG2 cells.
