Your browser doesn't support javascript.
loading
Effect and Mechanism of RBM8A on Proliferation, Migration and Apoptosis of Human Endometrial Cancer HEC-1A Cells / 肿瘤防治研究
Article en Zh | WPRIM | ID: wpr-986675
Biblioteca responsable: WPRO
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.
Palabras clave
Texto completo: 1 Base de datos: WPRIM Idioma: Zh Revista: Cancer Research on Prevention and Treatment Año: 2023 Tipo del documento: Article
Texto completo: 1 Base de datos: WPRIM Idioma: Zh Revista: Cancer Research on Prevention and Treatment Año: 2023 Tipo del documento: Article