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


ABSTRACT: 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.

SUBMITTER: Zhang T 

PROVIDER: S-EPMC5746364 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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

Zhang Tengyue T   Ma Kelong K   Huang Jin J   Wang Shitang S   Liu Yabei Y   Fan Gaofei G   Liu Miao M   Yang Guangshan G   Wang Cheng C   Fan Pingsheng P  

Oncotarget 20171026 66


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 prom  ...[more]

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