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Overexpression of MicroRNA-34a-5p Inhibits Proliferation and Promotes Apoptosis of Human Cervical Cancer Cells by Downregulation of Bcl-2

Aberrant expressions of microRNAs (miRNAs) are involved in the development and progression of various types of cancers. In this study, we investigated the roles of miR-34a-5p in the proliferation, migration, invasion, and apoptosis of cervical cancer cells (HeLa cells). We found that overexpression...

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Detalles Bibliográficos
Autores principales: Wang, Xiufen, Xie, Yucui, Wang, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cognizant Communication Corporation 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7844734/
https://www.ncbi.nlm.nih.gov/pubmed/28893346
http://dx.doi.org/10.3727/096504017X15037506066252
Descripción
Sumario:Aberrant expressions of microRNAs (miRNAs) are involved in the development and progression of various types of cancers. In this study, we investigated the roles of miR-34a-5p in the proliferation, migration, invasion, and apoptosis of cervical cancer cells (HeLa cells). We found that overexpression of miR-34a-5p significantly inhibited the viability, migration, and invasion of HeLa cells, but promoted cell apoptosis. Suppression of miR-34a-5p showed opposite effects. The mRNA and protein expression levels of Bcl-2 in HeLa cells were increased by miR-34a-5p suppression but decreased by miR-34a-5p overexpression. Bcl-2 was a direct target gene of miR-34a-5p, which participated in the effects of miR-34a-5p on HeLa cell viability, migration, invasion, and apoptosis. Suppression of miR-34a-5p promoted the viability, migration, and invasion of HeLa cells by increasing the expression of Bcl-2. Moreover, overexpression of Bcl-2 significantly promoted cell viability, migration, and invasion and had no influence on cell apoptosis. Suppression of Bcl-2 showed the opposite effects, with an increase in apoptosis. Overexpression of Bcl-2 activated the PI3K/AKT and JAK/STAT pathways in cervical cancer cells. Suppression of Bcl-2 inactivated the PI3K/AKT and JAK/STAT pathways in cervical cancer cells.