首页> 中文期刊> 《宁夏医科大学学报》 >AMPK激活对人胃癌SGC7901细胞上皮-间质转化和迁移侵袭能力的影响

AMPK激活对人胃癌SGC7901细胞上皮-间质转化和迁移侵袭能力的影响

         

摘要

目的 探讨腺苷酸活化蛋白激酶(adenosine monophosphate activated protein kinase,AMPK)激活对人胃癌SGC7901细胞上皮-间质转化(epithelial-mesenchymal transition,EMT)、迁移和侵袭能力的影响.方法 分别将10mmol·L-1二甲双胍(metformin)、2mmol ·L-1 5-氨基咪唑-4-甲酰胺核苷酸(5-amino-imidazole-4-carboxamide nucleotide,AICAR)、10μmol·L-1 compound C作用于人胃癌SGC7901细胞24h后,应用划痕愈合实验、Transwell小室法分别检测细胞的迁移和侵袭能力的变化,同时应用Westem blot法检测EMT相关分子标志物E-cadherin、Vimentin、α-SMA蛋白的表达水平.结果 二甲双胍、AICAR作用于SGC7901细胞24h后,p-AMPK蛋白表达上调(P均<0.01),细胞迁移和侵袭能力减弱(P均<0.05),E-cadherin蛋白表达上调(P均<0.001),Vimentin和α-SMA蛋白表达下调(P均<0.001);应用compound C作用于SGC7901细胞24h后,p-AMPK蛋白表达下调(P<0.01),细胞迁移和侵袭能力增强(P均<0.05),EMT分子标记物E-cadherin表达下调(P<0.001),Vimentin和α-SMA表达上调(P均<0.001).结论 AMPK激活可抑制人胃癌SGC7901细胞上皮-间质转化,并抑制其迁移和侵袭能力.%Objective To investigate the effects of adenosine monophosphate activatedprotein kinase (AMPK) activation on epitheliall-mesenchymal transition (EMT),migration and invasion in human gastric cancer SGC7901 cells.Methods Human gastric caner SGC7901 cells were treated with 10 mmol ·L-1 metformin,2mmol·L-1 AICAR and 10μmol· L-1 compound C.Cell migration and invasion ability were determined by the wound healing assay and Transwell chamber assay.The expression of total AMPK,phosphorylated AMPK (p-AMPK) and epithelial-mesenchymal transition (EMT)-related markers (E-cadherin 、Vimentin and α-SMA) were validated by Western blot.Results The expression of p-AMPK was increased significantly in metformin and AICAR groups compared with control group(Pall<0.01)while the ability of cell migration and invasion were decelerated significantly (P<0.05).Epithelial marker (E-cadherin) showed upexpression and mesenchymal markers (Vimentin,α-SMA) showed downexpression (P<0.001).On the contrary,the expression of p-AMPK was decreased in compound C group compared with control group (P<0.01) while the ability of cell invasion and migration were accelerated (P<0.01).Epithelial marker (E-cadherin) was downexpression and mesenchymal markers (Vimentin,α-SMA) were upexpression (P <0.001).Conclusion AMPK activation can inhibit the epithelial-mesenchymal transition,migration and invasion of human gastric cancer SGC7901 cells.

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