CDKN2B is critical for verapamil-mediated reversal of doxorubicin resistance in hepatocellular carcinoma

In this study, we explored the function and mechanism of CDKN2B genes in verapamil (VER)-induced reversal of resistance to doxorubicin (ADM) chemotherapy in hepatocellular carcinoma (HCC). We examined 4 HCC cell lines and found that the expression levels of CDKN2B genes correlated with the level of...

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Detalles Bibliográficos
Autores principales: Zhang, Tengyue, Ma, Kelong, Huang, Jin, Wang, Shitang, Liu, Yabei, Fan, Gaofei, Liu, Miao, Yang, Guangshan, Wang, Cheng, Fan, Pingsheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Research Paper
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5746364/
https://www.ncbi.nlm.nih.gov/pubmed/29299129
http://dx.doi.org/10.18632/oncotarget.22123
Descripción
Sumario:In this study, we explored the function and mechanism of CDKN2B genes in verapamil (VER)-induced reversal of resistance to doxorubicin (ADM) chemotherapy in hepatocellular carcinoma (HCC). We examined 4 HCC cell lines and found that the expression levels of CDKN2B genes correlated with the level of apoptosis induced by ADM+VER. Overexpression of CDKN2B genes promoted apoptosis in cells treated with VER+ADM. CDKN2B knockdown using siRNA weakened the effect of ADM+VER, indicating that ADM+VER promotes HCC cell apoptosis and that CDKN2B genes participate in VER-mediated promotion in tumor cell apoptosis. Future research will further explore the functional mechanism, and the associated signal transduction pathways via which CDKN2B affects HCC drug resistance.

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