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目的探讨阿霉素在胃癌细胞中诱导PI3′K/Akt/FKHRL1通路的激活,对胃癌细胞SGC-7901化疗效果的影响及两者的关系。方法2004-01~2005-09武汉大学人民医院消化内科采用MTT比色法检测胃癌细胞的生存率,Western印迹法检测FKHRL1磷酸化表达水平,同时观察PI3′K/Akt抑制剂wortmannin对阿霉素诱导的上述变化的影响。结果阿霉素抑制胃癌细胞SGC-7901的生长,呈时间依赖性的诱导FKHRL1磷酸化。wortmannin可明显增强阿霉素的细胞生长抑制作用,同时下调阿霉素诱导的磷酸化FKHRL1表达。结论阿霉素可能是通过激活SGC-7901细胞的PI3′K/Akt通路,呈时间依赖性诱导FKHRL1磷酸化,从而影响胃癌细胞的化疗耐药性。wortmannin可以阻断PI3′K/Akt/FKHRL1通路而提高胃癌的化疗敏感性。
Objective To investigate the effects of doxorubicin on the activation of PI3’K / Akt / FKHRL1 pathway in gastric cancer cells and the effect of chemotherapy on gastric cancer cells SGC-7901 and their relationship. Methods The survival rate of gastric cancer cells was detected by MTT colorimetric method in the Department of Gastroenterology, People’s Hospital of Wuhan University from January 2004 to September 2005. The phosphorylation of FKHRL1 was detected by Western blotting. The effect of PI3’K / Akt inhibitor wortmannin on doxorubicin The effects of these changes were induced. Results Adriamycin inhibited the growth of gastric cancer cell SGC-7901 and induced the phosphorylation of FKHRL1 in a time-dependent manner. wortmannin can significantly enhance the doxorubicin cytostatic effect, while down-regulating doxorubicin-induced phosphorylated FKHRL1 expression. Conclusion Adriamycin may affect the chemoresistance of gastric cancer cells by activating PI3’K / Akt pathway of SGC-7901 cells in a time-dependent manner to induce phosphorylation of FKHRL1. wortmannin can block the PI3’K / Akt / FKHRL1 pathway and improve the chemosensitivity of gastric cancer.