Let-7b inhibit or promote c-Myc via ATF6-induced Endoplasmic reticulum stress
Background: The development of multidrug resistance (MDR) in gastric cancer is the major cause of failure in chemotherapy and the high mortality but the mechanism behind it remains unclear.To clarify the mechanism between let-7b and c-myc is necessary.Method: The IC50 of 5-FU and cisplatin of SGC7901, SGC7901/DDP gastric cancer cells were used by an CCK8 assay.The expression of let-7b in SGC7901 and SGC7901/DDP cells was evaluated by qPCR and the expression of ATF6, CHOP, c-myc, GRP78 was evaluated by western blot analysis.The effect of apotosis of let-7b on cisplatin and 5-Fu induced apoptosis was investigated by annexin-V/PI flow cytometry.Results:The results from this study show that there is a possible pathway between let-7b and c-myc.In molecular studies, western blotting revealed that the transfection of let-7b could inhibit expression of c-Myc, ATF6 and GRP78.RT-PCR confirmed that the expression of c-myc decreased after transfected with let-7b.Conclusion:let-7b may interfere with the expression of c-myc by regulating the ATF6 —GRP78—CHOP pathway and ER stress-induced apotosis.
Gastric cancer apotosis ER-stress c-myc let-7b ATF6
Yupeng Zhang Hui Cai Xiaojun Yang Haizhong Ma Shixun Ma Xiangdong Niu Yifeng Chen
General surgery clinical center of Gansu province, Lanzhou, 730000, China
国内会议
兰州
英文
543-552
2016-10-01（万方平台首次上网日期，不代表论文的发表时间）