大黄素对胃癌细胞增殖、凋亡及ERK1/2-PKM2/P53通路的影响

Effects of Emodin on the Proliferation and Apoptosis of Gastric Cancer Cells and ERK1/2-PKM2/P53 Pathway

目的:探讨大黄素对胃癌细胞增殖、凋亡及ERK1/2-PKM2/P53通路的影响。方法:实验分为MGC803胃癌细胞组、氟尿嘧啶组、大黄素低剂量组、大黄素高剂量组,测定并比较各组细胞癌细胞活力、癌细胞单克隆形成数目、癌细胞凋亡率、穿膜孔数、以及MGC803胃癌细胞ERK1/2、PKM2、P53mRNA、蛋白水平。结果:与MGC803细胞组比较,氟尿嘧啶组、大黄素低、高剂量组吸光度(A)值、存活率水平、克隆形成数目、穿膜数、p-ERK1/2、p-PKM2 mRNA及蛋白表达水平降低,凋亡率、P53mRNA及蛋白表达水平升高(P<0.05)。与氟尿嘧啶组比较,大黄素低剂量组A值、存活率水平、克隆形成数目、穿膜数、pERK1/2、p-PKM2 mRNA、蛋白升高,凋亡率、P53 mRNA、蛋白表达水平降低(P<0.05)。与大黄素低剂量组比较,大黄素高剂量组A值、存活率、细胞克隆形成数目、穿膜数、P-ERK1/2及P-PKM2 mRNA及蛋白表达水平明显降低,凋亡率、P53 mRNA及蛋白表达水平明显升高(P<0.05)。结论:大黄素可能通过抑制ERK1/2-PKM2通路诱导P53高表达从而抑制胃癌细胞的增殖及迁徙,促进胃癌细胞的凋亡。

Objective:To investigate the effects of emodin on the proliferation and apoptosis of gastric cancer cells and ERK1/2-PKM2/P53 pathway.Methods:MGC803 gastric cancer cell group,5-fluorouracil group,emodin low-dose group and emodin high-dose group were set up.The cell viability,number of monoclonal formation,apoptotic rate of cancer cells,number of perforation,and ERK1/2,PKM2,P53 gene and protein levels of MGC803 gastric cancer cell were determined.Results:Compared with those in MGC803 cell group,the A value,survival rate,number of clone formation,transmembrane number,p-ERK1/2,p-PKM2 mRNA,protein expression levels in 5-fluorouracil group and emodin low and high dose groups were decreased,the mortality rate,P53 mRNA and protein expression levels were increased(P<0.05).Compared with those in 5-fluorouracil group,the OD value,survival rate,number of clone formation,transmembrane number,p-ERK1/2,p-PKM2 mRNA,protein elevation in the low dose group of emodin were increased,and the apoptosis rate,P53 mRNA and protein were decreased(P<0.05).Compared with those in the low dose group of emodin,the A value,survival rate,number of clone formation,number of transmembrane,p-ERK1/2,p-PKM2,mRNA protein expression were decreased,and the apoptosis rate,P53 mRNA and protein were increased(P<0.05).Conclusion:Emodin may inhibit the proliferation and migration of gastric cancer cells by inhibiting the high expression of P53 through inhibiting ERK1/2-PKM2 pathway,which promotes the apoptosis of gastric cancer cells.