CDKN2B is critical for verapamil-mediated reversal of doxorubicin resistance in hepatocellular carcinoma
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Tengyue Zhang1,2,*, Kelong Ma3,*, Jin Huang2,*, Shitang Wang4,*, Yabei Liu2, Gaofei Fan2, Miao Liu2, Guangshan Yang2, Cheng Wang4 and Pingsheng Fan1,2
1School of Clinical Medicine, Shan Dong University, Jinan 250100, China
2The Cancer Hospital of Anhui Province, Provincial Hospital of Anhui Medical University, Hefei 230032, China
3Clinical College of Integrated Traditional Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei 230032, China
4Department of General Surgery, Provincial Hospital of Anhui Medical University, Hefei 230032, China
*These authors have contributed equally to this work
Pingsheng Fan, email: firstname.lastname@example.org
Cheng Wang, email: email@example.com
Keywords: hepatocellular carcinoma (HCC); verapamil (VER); doxorubicin (ADM); CDKN2B; chemotherapy resistance
Received: June 14, 2017 Accepted: October 05, 2017 Published: October 26, 2017
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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