木黄酮靶向抑制MKN-45胃癌细胞Notch1蛋白表达及对增殖和凋亡的影响

目的:探讨木黄酮靶向抑制Notch1蛋白表达对人胃癌细胞MKN-45增殖和侵袭作用的影响及可能机制。方法:通过不同浓度木黄酮干预胃癌细胞MKN-45,以未干预细胞为正常对照组,Western blot法检测木黄酮抑制Notch1蛋白表达的效果,MTT法检测各组MKN-45细胞的增殖能力,荧光双标流式细胞术检测各组MKN-45细胞的凋亡状况,RT-PCR检测Bcl-2和BaxmRNA的表达水平。结果:木黄酮干预MKN-45胃癌细胞后能明显抑制Notch1蛋白表达,同时抑制MKN-45细胞增殖,促进MKN-45细胞凋亡。木黄酮干预明显上调细胞凋亡相关基因Bcl-2和Bax mRNA水平。结论:木黄酮干预可靶向抑制胃癌细胞MKN-45Notch1蛋白表达,抑制胃癌细胞MKN-45增殖并促进凋亡,可能与其上调细胞凋亡相关基因Bcl-2和Bax mRNA有关。

Effect of genistein on proliferation and apoptosis of gastric cancer cell line MKN-45 via inhibited the expression of Notch1 protein

Objective:To investigate the effect of genistein on cell proliferation and apoptosis in vitro in gastric cancer cell line MKN-45.Methods:The gastric cancer cell line MKN-45 was treated with gradient concentration of genistein.The protein of Notch1 was determined by Western blotting,meanwhile proliferation of MKN-45 was determined with methabenzthiazuron(MTT) assay and poptosis of MKN-45 was determined with flow-cytometry assay after treatment.The mRNA expression of Bcl-2 and Bax were determined by RT-PCR.Results:Compared with the control group,the protein expressions of Notch1 in MKN-45 was significantly decreased after treatment with genistein.The growth of MKN-45 cells was inhibited significantly and the apoptosis of MKN-45 were up-regulated after treatment with genistein.Additionally,the mRNA expressions of Bcl-2 and Bax were obviously increased.Conclusion:Genistein can inhibited proliferation and increased apoptosis of gastric cell line MKN-45 through decreased the expression of Nothc1 protein.