siP4HA1经Akt/ERK信号通路抑制胃癌细胞增殖

siP4HA1 promotes gastric cancer cell proliferation via inhibiting Akt/ERK pathway

目的探讨P4HA1对胃癌发生发展的影响及分子机制。方法构建P4HA1干扰质粒,稳定转染胃癌MKN-28细胞株;采取Western blot验证P4HA1干扰效率;MTT检测P4HA1干扰前后细胞增殖变化;Western blot检测增殖相关蛋白Akt和ERK表达水平;通过裸鼠移植瘤模型探讨P4HA1对成瘤生长的影响。结果成功构建P4HA1干扰质粒并稳转胃癌MKN-28细胞株,P4HA1表达抑制后MKN-28细胞增殖受到抑制;Akt和ERK蛋白表达降低,移植瘤实验组中P4HA1干扰后裸鼠肿瘤生长受到抑制。结论P4HA1通过调节Akt和ERK途径促进胃癌细胞增殖。

Objective To investigate the effects of P4HA1 on development of gastric cancer cell and its molecular mechanism.Methods P4HA1 interfering plasmid was constructed to stabilize transfection of gastric cancer MKN-28 cell lines.Using Western blot to verify P4HA1 interference efficiency.MTT assay was used to detect cell proliferation before and after P4HA1 interference.Western blot detected the expression of proliferating related proteins Akt and ERK.Effect of P4HA1 on tumor growth in xenografted tumor model.Results P4HA1 interfering plasmid was successfully constructed and transfected into gastric cancer MKN-28 cell lines.The expression of Akt and ERK protein was reduced,and the growth of xenografted tumor after P4HA1 interference was inhibited compared with control group.Conclusion P4HA1 promotes the proliferation of gastric cancer cells by inhibiting Akt and ERK pathways.