摘要
目的:探讨糖原合成激酶-3β(glycogen synthase kinase-3β,GSK-3β)在内质网应激调控胃癌细胞侵袭中的作用。方法:以浓度为3μmol/L的衣霉素(Tunicamycin,TM)单独及联合运用浓度为10mmol/L的氯化锂(Lithium chloride,LiCl)处理胃癌SGC7901细胞24h,Transwell侵袭实验检测细胞侵袭能力,并应用Western blot检测GSK-3β蛋白Ser9位点的表达。结果:Transwell侵袭实验显示,联合运用TM+LiCl处理胃癌SGC7901细胞24h,可明显改善TM所诱导的内质网应激对细胞侵袭性力的影响;Western blot结果显示,相对于对照组,TM处理组Ser9-GSK-3β蛋白的表达明显降低,联合运用TM+LiCl,可明显升高Ser9-GSK-3β蛋白的表达,差异有统计学意义(P<0.01)。结论:抑制GSK-3β的表达,可通过降低内质网应激明显增强胃癌细胞的侵袭力。
Objective:To investigate the Role of GSK-3βin controlling gastric cancer cell invasion regula-ted by endoplasmic reticulum stress.Methods:TM (3μmol/L)alone or in combination with LiCl (10 mmol/L)was incubated with SGC7901 cells for 24h.After treatment,the invasion of gastric cancer cells was evalu-ated by Transwell chamber assays.The expression of GSK-3βat Ser9 were examined by Western blot analy-sis.Results:Transwell and Western blot showed that TM induced-endoplasmic reticulum stress decreased the invasion ability of gastric cancer SGC7901 cells and the phosphorylation of GSK-3βat Ser9.However,simul-taneous treatment with Lithium chloride (LiCl)increased the invasion of gastric cancer cells by counteracting the activating effect of TM on GSK-3β,causing an increase in the phosphorylation of Ser9-GSK-3β.The difference was statistically significant(P<0.01).Conclusion:Inhibiting the expression of GSK-3βmay increase the invasion of gastric cancer cells induced by endoplasmic reticulum stress.
出处
《数理医药学杂志》
2016年第4期480-482,共3页
Journal of Mathematical Medicine
基金
湖北省教育厅科研项目(B2014079)
国家自然科学基金青年项目(81402315)
武汉市教育局项目(2011065)
关键词
GSK-3Β
内质网应激
胃癌
侵袭
GSK-3β
endoplasmic reticulum stress
gastric cancer
invasion
