摘要
目的研究5-氨基咪唑-4-甲酰胺核苷酸(5-aminoimidazole-4-carboxamide ribonucleotide,AICAR)对人胃癌BGC823细胞增殖、迁移和侵袭能力的影响。方法分别将0.5、1、2和3mmol·L^(-1) AICAR作用于人胃癌BGC823细胞24、48和72h后,应用MTT法检测细胞增殖情况;Western blot法检测BGC823细胞内磷酸化腺苷酸活化蛋白激酶(phosphorylated-Adenosine monophosphate activated protein kinase,p-AMPK)蛋白的表达。2mmol·L^(-1) AICAR作用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;结果 MTT法检测结果显示,0.5、1、2和3mmol·L^(-1) AICAR分别作用24、48和72h后,人胃癌BGC823细胞的增殖能力均被抑制,随着AICAR作用浓度增加和作用时间的延长,对BGC823细胞抑制作用逐渐增强,呈时间和剂量依赖性(P均<0.01);与对照组相比,2mmol·L^(-1) AICAR作用后,BGC823细胞的迁移和侵袭能力均减弱(P均<0.01);随着AICAR作用浓度增加和作用时间延长,p-AMPK蛋白表达逐渐增加(P均<0.01)。结论 AICAR可抑制BGC823细胞的增殖、迁移和侵袭能力;AICAR通过上调BGC823细胞内p-AMPK蛋白表达而发挥肿瘤抑制作用。
Objective To investigate the effects of 5-aminoimidazole-4-carboxamide ribonucleotide（AICAR）on proliferation,migration and invasion in human gastric cancer BGC823 cells. Methods Cell proliferation after treatment with 0.5,1,2 and 3 mmol·L^-1 AICAR for 24,48 and 72 h were detected by MTT assay.Cell migration and invasion ability after treatment with 2 mmol·L^-1 AICAR for 24 h were determined by the wound healing assay and Transwell chamber assay.The expression of phosphorylated AMPK（p-AMPK） was validated by Western blotting. Results AICAR inhibited significantly the proliferation of BGC823 cells in a time and dose-dependent manner（P〈0.01）. The ability of cell migration and invasion was decelerated significantly（P〈0.01）. The expression of p-AMPK was increased significantly in a time and dose-dependent manner（P〈0.01）. Conclusion AICAR can inhibit the proliferation,migration and invasion of human gastric cancer BGC823 cells. AICAR upregulated p-AMPK protein expression.
出处
《宁夏医科大学学报》
2017年第9期994-997,1002,共5页
Journal of Ningxia Medical University
基金
国家自然科学基金(81460370)
宁夏自然科学基金(NZ13143
NZ15141)
宁夏医科大学校级项目(XQ2012008)
