“黄芪-莪术”药对通过PTEN与p-AKT对人乳腺癌细胞增殖的影响

Effects of“Radix Astragali seu Hedysari-Rhizoma Curcumae”on Proliferation of MDA-MB-231 Cells through PTEN and p-AKT

目的:探讨“黄芪-莪术”药对通过PTEN与p-AKT对人乳腺癌细胞(MDA-MB-231)增殖的作用机制。方法:将MDA-MB-231细胞进行“黄芪-莪术”药对(药对组)、顺铂(顺铂组)、“黄芪-莪术”药对联合顺铂(药对+顺铂组)治疗,并设置空白对照组。MTT法检测细胞增殖,RT-qPCR检测PTEN与p-AKT的mRNA表达水平,Western Blotting检测p-AKT蛋白表达水平。结果:与空白对照组比较,药对组PTEN mRNA表达水平上升,OD值与p-AKT蛋白表达水平下降(P<0.05),p-AKT mRNA蛋白表达水平变化差异无统计学意义(P>0.05);顺铂组OD值与PTEN mRNA表达水平下降(P<0.05),p-AKT mRNA与蛋白表达水平变化差异无统计学意义(P>0.05);而药对+顺铂组在药对治疗的基础上能进一步抑制MDA-MB-231细胞增殖,促进PTEN mRNA的表达,抑制p-AKT mRNA与蛋白表达水平。结论:“黄芪-莪术”药对抑制MDA-MB-231细胞增殖的机制可能通过上调PTEN基因而直接抑制AKT蛋白水平。

Objective:To explore the effects mechanism of“Radix Astragali seu Hedysari-Rhizoma Curcumae”on the proliferation of MDA-MB-231 cells through PTEN and p-AKT.Methods:MDA-MB-231 cells were treated with“Radix Astragali seu Hedysari-Rhizoma Curcumae”drug pair(drug pair group),cisplatin(cisplatin group),“Radix Astragali seu Hedysari-Rhizoma Curcumae”drug pair combined with cisplatin(drug pair+cisplatin group),and blank control group was set.Then,MTT method was used to detect cell proliferation,RT-qPCR was used to detect PTEN and p-AKT mRNA expression levels,and Western blot was used to detect p-AKT protein expression levels.Results:Compared with the blank control group,the PTEN mRNA expression level of the drug-pair group increased,the OD value and p-AKT protein expression level decreased(P<0.05),the p-AKT mRNA protein expression level did not change significantly(P>0.05);the OD value and PTEN mRNA expression level of the cisplatin group decreased(P<0.05),and the expression levels of p-AKT mRNA and protein did not change significantly(P>0.05);while the drug pair+cisplatin group could further improve on the basis of drug pair treatment Inhibit MDA-MB-231 cell proliferation,promote PTEN mRNA expression,and inhibit p-AKT mRNA and protein expression levels.Conclusion:The mechanism of“Radix Astragali seu Hedysari-Rhizoma Curcumae”drug on inhibiting MDA-MB-231 cell proliferation may directly inhibit AKT protein level by up-regulating PTEN gene.