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作 者:Jian Wang Xiaoqing Zeng Tiancheng Luo Wei Jin Shiyao Chen
机构地区:[1]Department of Gastroenterology and Hepatology,Zhongshan Hospital,Fudan University,Shanghai 200032,China [2]Department of Oncology,Breast Cancer Institute,Shanghai Cancer Center,Shanghai Medical College,Fudan University,Shanghai 200032
出 处:《Acta Biochimica et Biophysica Sinica》2012年第9期752-758,共7页生物化学与生物物理学报(英文版)
基 金:This study was supported by the grant from the National Natural Science Foundation of China (30200151 ).
摘 要:Over-expression of MDR1 confers multidrug resistance (MDR) in cancers and remains a major cause for the failure of chemotherapy. In the present study, we found that V-Ets erythroblastosis virus E26 oncogene homolog 2 (ETS2) could activate MDR1 transcription and P-glycoprotein (P-gp) expression in SGC7901 cells. Knockdown of ETS2 attenuated MDR1 transcription and P-gp expression, and increased the sensitivity of MDR cancer cells to cytotoxic drugs that were transported by P-gp in SGC7901/VCR cells. ETS2 could bind to the ETS2 sites on the MDR1 promoter and activate its transcription. The regulation of MDR1 expression by ETS2 may provide potential ways to overcome MDR in cancer treatment.Over-expression of MDR1 confers multidrug resistance (MDR) in cancers and remains a major cause for the failure of chemotherapy. In the present study, we found that V-Ets erythroblastosis virus E26 oncogene homolog 2 (ETS2) could activate MDR1 transcription and P-glycoprotein (P-gp) expression in SGC7901 cells. Knockdown of ETS2 attenuated MDR1 transcription and P-gp expression, and increased the sensitivity of MDR cancer cells to cytotoxic drugs that were transported by P-gp in SGC7901/VCR cells. ETS2 could bind to the ETS2 sites on the MDR1 promoter and activate its transcription. The regulation of MDR1 expression by ETS2 may provide potential ways to overcome MDR in cancer treatment.
关 键 词:multidrug resistance ETS2 MDR1
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