摘要
目的:研究芹菜素能否通过下调糖代谢相关激酶HK-2表达抑制体外培养非小细胞肺癌H460细胞糖酵解及自我更新能力.方法:HK-2 cDNA转染、亚细胞毒浓度的芹菜素(20μM、40μM和80μM)处理或芹菜素(80μM)联合HK-2 cDNA转染H460细胞.蛋白质印迹检测HK-2表达水平,检测乳酸产物和葡萄糖消耗水平,同时,球形成实验测验自我更新能力.结果:亚细胞毒浓度的芹菜素以剂量依赖趋势下调非小细胞肺癌H460细胞的糖代谢相关激酶HK-2表达和减少乳酸产物和葡萄糖消耗,并且降低球形成率.此外,过表达HK-2能救援芹菜素抑制非小细胞肺癌H460细胞乳酸产生、葡萄糖消耗以及球形成率作用.结论:芹菜素通过下调HK-2表达抑制非小细胞肺癌H460细胞糖酵解及自我更新能力.
Objective To investigate whether apigenin(API)inhibits the glycolysis and self-renewal capacity by downregulating the expression of glucose metabolism related kinase HK-2 in non-small cell lung cancer(NSCLC)H460 cells in vitro.Methods H460 cells were transfected with HK-2 cDNA,treated with sub-cytotoxicity concentrations of API(20μM;40μM and 80μM)or in combination with API(80μM)treatment and HK-2 cDNA transfection.Western blot was utilized to detect the expression of HK-2.The levels of lactate production and glucose consumption were using measurement of lactate production and glucose consumption assays.The spheroid formation assay was employed to detect the self-renewal capacity in H460 cells.Results The sub-cytotoxic concentrations of API decreased the expression of glucose metabolism related kinase HK-2 and reduced lactiate production and glucose consumption,as well as decreased sphere formation rate in NSCLC H460 cells in a dosedependent tendency.Moreover,overexpression of HK-2 could rescue the inhibitory effects of API on lactate production,glucose consumption and spheroid formation in NSCLC H460 cells.Conclusion API can inhibit glycolysis and self-renewal capacity by downregulating HK-2 expression in NSCLC H460 cells.
作者
孙菲
袁庆
张坚松
SUN Fei;YUAN Qing;ZHANG Jiansong(School of Medicine,Hunan Normal University,Changsha 410013,China)
出处
《湖南师范大学学报（医学版）》
2023年第1期1-5,12,共6页
Journal of Hunan Normal University(Medical Sciences)
基金
国家自然科学基金项目(No.81172375)
