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CDKN2B对于维拉帕米介导的肝癌多柔比星耐药逆转至关重要。

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

作者信息

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

机构信息

School of Clinical Medicine, Shan Dong University, Jinan 250100, China.

The Cancer Hospital of Anhui Province, Provincial Hospital of Anhui Medical University, Hefei 230032, China.

出版信息

Oncotarget. 2017 Oct 26;8(66):110052-110063. doi: 10.18632/oncotarget.22123. eCollection 2017 Dec 15.

DOI:10.18632/oncotarget.22123
PMID:29299129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5746364/
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.

摘要

在本研究中,我们探讨了细胞周期蛋白依赖性激酶抑制剂2B(CDKN2B)基因在维拉帕米(VER)诱导的肝癌(HCC)对阿霉素(ADM)化疗耐药逆转中的作用及机制。我们检测了4种肝癌细胞系,发现CDKN2B基因的表达水平与ADM+VER诱导的细胞凋亡水平相关。CDKN2B基因的过表达促进了VER+ADM处理的细胞凋亡。使用小干扰RNA(siRNA)敲低CDKN2B减弱了ADM+VER的作用,表明ADM+VER促进肝癌细胞凋亡,且CDKN2B基因参与VER介导的肿瘤细胞凋亡促进作用。未来的研究将进一步探索CDKN2B影响肝癌耐药性的功能机制及相关信号转导通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/50786317a2ef/oncotarget-08-110052-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/559b58f416c7/oncotarget-08-110052-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/52b75378a505/oncotarget-08-110052-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/093c5fec8ee1/oncotarget-08-110052-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/50cecc099b38/oncotarget-08-110052-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/352073f385e9/oncotarget-08-110052-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/548987768a28/oncotarget-08-110052-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/a29b4d637311/oncotarget-08-110052-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/3b226c55a1ee/oncotarget-08-110052-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/50786317a2ef/oncotarget-08-110052-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/559b58f416c7/oncotarget-08-110052-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/52b75378a505/oncotarget-08-110052-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/093c5fec8ee1/oncotarget-08-110052-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/50cecc099b38/oncotarget-08-110052-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/352073f385e9/oncotarget-08-110052-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/548987768a28/oncotarget-08-110052-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/a29b4d637311/oncotarget-08-110052-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/3b226c55a1ee/oncotarget-08-110052-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b9af/5746364/50786317a2ef/oncotarget-08-110052-g009.jpg

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