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Sulindac sulfide selectively increases sensitivity of ABCC1 expressing tumor cells to doxorubicin and glutathione depletion

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The Journal of Biomedical Research 2016年第2期30卷 120-133页

作者： Jason D.Whitt Adam B.Keeton Bernard D.Gary larry a.sklar Kamlesh Sodani Zhe-Sheng Chen Gary A.Piazza Department of Biochemistry University of Mississippi Medical Center Cancer Institute Jackson MS 39216 USA Drug Discovery Research Center Mitchell Cancer Institute University of South Alabama Mobile AL 36604 USA ADT Pharmaceuticals Inc. Orange Beach AL 36561 USA Department of Pathology The University of New Mexico Albuquerque NM87131 USA Department of Pharmaceutical Sciences St. John's University New York NY 11439 USA

ATP-binding cassette（ABC） transporters ABCC1（MRP1）,ABCB1（P-gp）,and ABCG2（BCRP） contribute to chemotherapy *** primary goals of this study were to characterize the efficacy and mechanism of the nonsteroidal anti-inflammatory drug（NSAID）,sulindac sulfide,to reverse ABCC1 mediated resistance to chemotherapeutic drugs and to determine if sulindac sulfide can influence sensitivity to chemotherapeutic drugs independently of drug *** assays were performed to measure resistance of ABC-expressing cell lines to doxorubicin and other chemotherapeutic *** were tested for the ability to restore sensitivity to resistance selected tumor cell lines,as well as a large panel of standard tumor cell *** experiments characterized the mechanism by which sulindac sulfide inhibits ABCC1 substrate and co-substrate（GSH） transport in isolated membrane vesicles and intact *** reversal of multi-drug resistance（MDR）,decreased efflux of doxorubicin,and fluorescent substrates were demonstrated by sulindac sulfide and a related NSAID,indomethacin,in resistance selected and engineered cell lines expressing ABCC 1,but not ABCB 1 or *** sulfide also inhibited transport of leukotriene C_4 into membrane *** sulfide enhanced the sensitivity to doxorubicin in 24 of 47 tumor cell lines,including all melanoma lines tested（7-7）.Sulindac sulfide also decreased intracellular GSH in ABCC1 expressing cells,while the glutathione synthesis inhibitor,BSO,selectively increased sensitivity to sulindac sulfide induced *** sulfide potently and selectively reverses ABCC1-mediated MDR at clinically achievable ***1 expressing tumors may be highly sensitive to the direct cytotoxicity of sulindac sulfide,and in combination with chemotherapeutic drugs that induce oxidative stress.

关键词： multi-drug resistance doxorubicin sulindac MRP1 glutathione

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