Effect and Mechanism of RBM8A on Proliferation, Migration and Apoptosis of Human Endometrial Cancer HEC-1A Cells
10.3971/j.issn.1000-8578.2023.22.0705
- VernacularTitle:RBM8A基因对子宫内膜癌HEC-1A细胞增殖、迁移和凋亡的作用及其机制
- Author:
Dongmei TAN
1
;
Jingjing ZHANG
;
Yimin SHI
;
Sai HAN
;
Wei GENG
;
Jianyi SUN
;
Yayu WANG
;
Xiurong ZHANG
Author Information
1. TCM Gynecology, Shandong Provincial Maternal and Child Health Care Hospital, Ji'nan 250000, China
- Publication Type:Research Article
- Keywords:
Human endometrial cancer;
RBM8A;
Proliferation;
Migration;
Apoptosis;
Epithelial-mesenchymal transition
- From:
Cancer Research on Prevention and Treatment
2023;50(1):27-32
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of silenced RBM8A gene on the biological behavior (proliferation, migration, and apoptosis) of human endometrial cancer HEC-1A cells and its possible mechanism. Methods The hairpin shRNA targeted by the RBM8A gene was designed, and the best shRNA silencing fragment was screened. The recombinant lentiviral interference vector carrying the target gene was constructed and used to infect HEC-1A cells. Cells with stable knockdown of RBM8A gene were screened by puromycin as the experimental group (shRBM8A), while the shRNA of nonsense sequence was designed as the control group (shControl). CCK-8 method was used to detect cell proliferation, and flow cytometry was used to detect cell apoptosis. Transwell assay was used to detect cell migration and invasion. Western blot was used to analyze the expression of apoptosis-related proteins and EMT signal transduction pathway related proteins. Results In comparison with the shControl group, after RBM8A knockdown, HEC-1A cell proliferation was reduced, apoptosis was increased, migration and invasion ability were significantly inhibited (P < 0.05), the expression of apoptosis-related proteins cleaved caspase 9 and caspase 3 increased, EMT-related protein E-cadherin expression increased, and Vimentin expression decreased. Conclusion RBM8A gene silencing can inhibit the proliferation, migration, and invasion and promote the apoptosis of endometrial cancer cells. The inhibition of EMT signal transduction pathway may be its mechanism.
