Rg3通过PI3K/Akt调控MGBA表达促进乳腺癌细胞凋亡的研究

Studies on Mechanisms of Rg3 Inducing Apoptosis through PI3K / Akt Mediating MGBA in Breast Cancer Cells

目的研究人参皂甙Rg3是否是通过PI3K/Akt信号通路来抑制MGBA的表达,进而促进乳腺癌MDA-MB-231细胞的凋亡。方法实验分组:40 nmol/L IGF-1组、100 ng/m L Rg3组、IGF-1+Rg3组和空白对照组。Western-blot检测人参皂苷Rg3对乳腺癌MDA-MB-231细胞内p-Akt及MGBA蛋白表达的影响。MTT法检测作用48 h后人参皂苷Rg3对乳腺癌MDA-MB-231细胞增殖的抑制程度;流式细胞术检测作用48 h后人参皂苷Rg3对乳腺癌MDA-MB-231细胞凋亡的影响。结果 Trans well检测结果显示:Rg3可以抑制乳腺癌MDA-MB-231细胞中MGBA的表达,但当增强p-Akt的表达时Rg3的这种抑制作用被明显降低;MTT法检测结果显示:与空白对照组比较,IGF-1组和IGF-1+Rg3组明显促进细胞增殖,而Rg3组明显抑制细胞增殖;流式细胞术检测结果显示:与空白对照组比较,IGF-1组和IGF-1+Rg3组细胞凋亡率明显降低,而Rg3组细胞凋亡率明显增强。结论人参皂甙Rg3干扰乳腺癌细胞内MGBA的表达来促进乳腺癌细胞凋亡的作用是通过影响PI3K/Akt信号通路活性来得以实现的。

Objective To study whether ginsenoside Rg3 inhibits the expression of MGBA through PI3K/Akt signaling pathway and then promotes the apoptosis of breast cancer MDA-MB-231 cells. Methods Experimental groups：40 nmol/L IGF-1 group, 100 ng/mL Rg3 group, IGF-1＋Rg3 group and control group. Western-blot tested the effect of Rg3 on the expression of p-Akt and MGBA in breast cancer MDA-MB-231cells. MTT assay tested the inhibition of proliferation of Rg3 on breast cancer MDA-MB-231cell after 48 hours. Flow cytometry assay tested the effect of Rg3 on apoptosis of breast cancer MDA-MB-231cells after 48 hours. Results Trans well test results show that Rg3 can inhibit the expression of MGBA in breast cancer MDA-MB-231cells, but the effect can be significantly inhibited when the p-Akt expression is enhanced; MTT assay test results show：compared with control group, IGF-1 group and IGF-1 ＋ Rg3 group significantly promoted cell proliferation while Rg3 group significantly inhibited cell proliferation. Flow cytometry shows：compared with the control group, the apoptosis rates of IGF-1 group and IGF-1＋ Rg3 group significantly de-crease while apoptosis rate in the Rg3 group is significantly enhanced. Conclusion It is through impacting on PI3K / Akt signaling pathway that ginsenoside Rg3 disturbs the expression of MGBA to promote the apoptosis of breast cancer cells.