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Deregulation of microRNA-193b affects the proliferation of liver cancer via myeloid cell leukemia-1

Deregulation of microRNA (miR)-193b has been revealed to be associated with the proliferation of liver cells. However, the interaction between miR-193b and their targets inducing liver cancer remains largely unknown. The aim of the present study was to investigate the hypothesis that miR-193b affect...

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Detalles Bibliográficos
Autores principales: Yin, Wenjun, Nie, Yuehua, Chen, Lingying, Wang, Quipping, Liu, Shuangquan, He, Xiusheng, Wang, Wenjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5778835/
https://www.ncbi.nlm.nih.gov/pubmed/29435004
http://dx.doi.org/10.3892/ol.2017.7690
Descripción
Sumario:Deregulation of microRNA (miR)-193b has been revealed to be associated with the proliferation of liver cells. However, the interaction between miR-193b and their targets inducing liver cancer remains largely unknown. The aim of the present study was to investigate the hypothesis that miR-193b affects the proliferation of liver cancer cells. In the present study, the overall survival of patients with liver cancer and low fold change of miR-193b was higher compared with that of patients with liver cancer patients and high fold change of miR-193b. The expression level of myeloid cell leukemia-1 (Mcl-1) in patients with liver cancer was lower compared with in the control group. The results of the present study demonstrated that downregulation of miR-193b suppressed the proliferation and induced apoptosis of liver cancer cells, and inhibited the Mcl-1 protein expression level in liver cancer cells. Upregulation of miR-193b increased cell proliferation and decreased apoptosis of liver cancer cells and promoted the expression level of Mcl-1 protein. The results of the present study demonstrated that the expression of miR-193b as a novel tumor suppressor serves an important role in the proliferation of liver cancer cells by mediating Mcl-1 expression.