Data showing the circumvention of oxaliplatin resistance by vatalanib in colon cancer

被引:6
|
作者
To, Kenneth K. W. [1 ]
Poon, Daniel C. [1 ]
Wei, Yuming [1 ]
Wang, Fang [2 ]
Lin, Ge [3 ]
Fu, Li-wu [2 ]
机构
[1] Chinese Univ Hong Kong, Sch Pharm, Fac Med, Hong Kong, Peoples R China
[2] Sun Yat Sen Univ, State Key Lab Oncol South China, Canc Ctr, Guangzhou, Guangdong, Peoples R China
[3] Chinese Univ Hong Kong, Sch Biomed Sci, Fac Med, Hong Kong, Peoples R China
来源
DATA IN BRIEF | 2016年 / 7卷
基金
中国国家自然科学基金;
关键词
Vatalanib; Tyrosine kinase inhibitor; Oxaliplatin; Platinum drugs; Chemoresistance;
D O I
10.1016/j.dib.2016.02.064
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
We have recently reported that vatalanib, an orally active small molecule multi-tyrosine kinase inhibitor (Hess-Stumpp et al., 2005 [1]), can sensitize multidrug resistant (MDR) colon cancer cells to chemotherapy under hypoxia by inhibiting two MDR transporters ABCB1 and ABCG2 (To et al., 2015 [2]). This data article describes the possible circumvention of resistance to specifically platinum (Pt)-based anticancer drugs by vatalanib via inhibition of two other efflux transporters ABCC2 and ATP7A. Data from the flow cytometric transporter efflux assay showed specific inhibition of ABCC2 activity by vatalanib in stable transfected cells and ABCC2overexpressing oxaliplatin-resistant colon cancer cells HCT116/ Oxa. We also performed the transporter ABCC2 ATPase assay and showed an increase in ATP hydrolysis by ABCC2 in the presence of vatalanib. ATP7A mRNA expression was also shown to be upregulated in HCT116/0xa cells. Vatalanib was shown to suppress this upregulated ATP7A expression. Data from the cellular Pt accumulation assay showed a lower Pt accumulation in HCT116/0xa cells than the parental sensitive HCT116 cells. Vatalanib was shown to increase cellular Pt accumulation in a concentration-dependent manner. Combination of oxaliplatin and vatalanib was shown to restore the suppressed apoptosis in HCT116/0xa cells. (C) 2015 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/40).
引用
收藏
页码:437 / 444
页数:8
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