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

نویسندگان

  • Tengyue Zhang
  • Kelong Ma
  • Jin Huang
  • Shitang Wang
  • Yabei Liu
  • Gaofei Fan
  • Miao Liu
  • Guangshan Yang
  • Cheng Wang
  • Pingsheng Fan
چکیده

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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عنوان ژورنال:

دوره 8  شماره 

صفحات  -

تاریخ انتشار 2017