D氨基葡萄糖衍生物通过JNK信号通路诱导Eca109细胞凋亡
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Apoptosis in human esophageal cancer cell line Eca109 induced by the derivative of Dglucosamine via JNK signaling pathwayQIANG ZhanRong, WU Jing, ZHOU YongNing, LI Juan, YANG GuoDong, WANG AiQing, XUE QunJi
1Department of Gastroenterology, First Hospital, Lanzhou University
2Lanzhou Institute of Physics and Chemistry, Chinese Academy of Sciences, Lanzhou 730000, China
【Abstract】 AIM: To investigate the role of cjun Nterminal kinase (JNK) signaling pathway in the apoptosis of human esophageal cancer Eca109 cells induced by the derivative of Dglucosamine ({2(3carboxy1oxopropyl)amino2deoxyDGlucose}, COPADG) and the possible mechanisms. METHODS: Eca109 cells were cultured in vitro by using RPMI1640 and calf serum. Eca109 cells were preincubated with SP600125 for 30 min prior to exposure to COPADG at different concentrations and for different time. Changes in expression of PJNK protein were examined by Western Blot; cell growth inhibitory rate was detected by MTT colorimetric assay; the cell morphological changes were observed by inverted phase contrast microscopy. Apoptosis rate was analyzed by using Annexin V/PI fluorescence staining together with flow cytometry. RESULTS: COPADG could significantly inhibit the proliferation of Eca109 cells and induce their apoptosis. Western Blot showed that the protein expression of PJNK was increased in a dosedependent manner in Eca109 cells after stimulated by COPADG. SP600125 remarkablely decreased the protein expression of PJNK as well as the apoptosis rate and cell growth inhibitory rate in Eca109 cells induced by COPADG as compared with those treated with only COPADG. CONCLUSION: JNK signaling pathway may play an important role in the apoptosis of Eca109 cells following COPADG treatment. ......
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