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作 者:Xue-kai PAN Fei SU Li-hua XU Zhang-shuo YANG Dan-wen WANG Li-jie YANG Fan-zheng KONG Wei XIE Mao-hui FENG
机构地区:[1]Department of Gastrointestinal Surgery,Zhongnan Hospital of Wuhan University,Wuhan 430071,China [2]Department of Oncology,the First Hospital oJ'Lanzhou University,Lanzhou 730000,China
出 处:《Current Medical Science》2018年第6期1018-1024,共7页当代医学科学(英文)
基 金:grants from the National Natural Science Foundation of China(No.81072152 and No.81770283);Natural Science Foundation of Hubei Province(No.2015CFA027);Research Foundation of Health and Family Planning Commission of Hubei Province(No.WJ2015MA010 and No.WJ2017M249);Clinical Medical Research Center of Peritoneal Cancer of Wuhan (No.2015060911020462).
摘 要:Epirubicin,which is a conventional chemotherapeutic drug for gastric cancer,has innate and adaptive chemoresistance.Recent studies revealed that epirubicin could induce autophagy as a defensive mechanism in drug resistance of mammary carcinoma.Another study implied that D J-1 may be a chemoresistance-related gene.But the association between D J-1 and drug resistance of epirubicin in gastric cancer is still ambiguous.In the present report,we explored whether and how D J-1 conduced to epirubicin-induced apoptosis in gastric cancer.Epirubicin dose-dependently increased the expression of DJ-1 and induced autophagy.Knockdown of DJ-1 notably enhanced epirubicin-induced cell apoptosis,whereas overexpression of DJ-1 attenuated epirubicin-induced cell apoptosis.Further studies revealed that down-regulation of DJ-1 modulated epirubicin-activated autophagy which augmented epirubicin-induced apoptosis.In conclusion,our results validated that DJ-1 reduced epirubicin-induced apoptosis in gastric cancer cells via modulating epirubicin-activated autophagy.
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