人参皂苷Rg3 通过PI3K/AKT 信号系统调控CaM 基因表达促进胃癌BGC-823 细胞的凋亡

[摘要] 目的：探讨人参皂甙Rg3 通过PI3K/AKT信号通路干扰CaM基因的表达及对胃癌BGC-823 细胞凋亡的影响。方法:胃癌BGC-823 细胞的培养与传代完成后，Western blotting 检测胰岛素样生长因子-1 (insulin-like growth factor-1，IGF-1)和/或Rg3分别作用胃癌BGC-823 细胞后p-AKT和CaM 蛋白表达水平，MTT法检测IGF-1 和/或Rg3 对胃癌BGC-823 细胞增殖的影响，Transwell 法检测IGF-1 和/或Rg3 对胃癌BGC-823 细胞侵袭的影响，流式细胞术检测IGF-1 和/或Rg3 对胃癌BGC-823 细胞凋亡的影响。结果：随着IGF-1 作用时间延长，胃癌BGC-823 细胞中p-AKT蛋白和CaM蛋白的表达水平均明显提高（均P<0.05）；与空白对照组比较，Rg3 组明显抑制胃癌BGC-823 细胞增殖，而IGF-1 组和IGF-1+Rg3 组明显促进胃癌BGC-823 细胞增殖（均P<0.05）；与空白对照组比较，Rg3 组明显降低胃癌BGC-823 细胞侵袭，而IGF-1 组和IGF-1+Rg3 组明显促进胃癌BGC-823 细胞侵袭能力（均P<0.05）；流式细胞术检测显示，与空白对照组比较，Rg3 组明显促进胃癌BGC-823 细胞凋亡，而IGF-1 组和IGF-1+Rg3 组明显抑制胃癌BGC-823 细胞凋亡（均P<0.05）。结论:人参皂甙Rg3 通过阻断PI3K/AKT信号通路来抑制CaM的表达，进而促进胃癌BGC-823细胞的凋亡。

Ginsenoside Rg3 regulates CaM gene expression through PI3K/AKT signal system to promote apoptosis of gastric cancer BGC-823 cell

[Abstract] Objective: To investigate Ginsenoside Rg3 interfering the expression of CaM through PI3K/AKT signaling pathway to affect the biological activity of gastric cancer BGC-823 cells. Methods: After the culture and passage of gastric cancer BGC-823 cells,Western blotting was used to detect the expression of p-AKT and CaM protein in gastric cancer BGC-823 cells treated with IGF-1 and/or Rg3; The effect of IGF-1 and/or Rg3 on the proliferation of BGC-823 cells was detected by MTT assay; The effect of IGF-1 and/or Rg3 on the invasion of BGC-823 cells was detected by Transwell assay; Effect of IGF-1 and/or Rg3 on apoptosis of BGC-823 cells was detected by Flow Cytometry. Results: Western blotting results showed that the expression of p-AKT and CaM protein increased in BGC-823 cells with the prolongation of IGF-1 treatment (all P<0.05); Compared with the blank control group, Rg3 significantly inhibited the proliferation of BGC-823 cells, while IGF-1 and IGF-1+Rg3 significantly promoted the cell proliferation (all P<0.05); Compared with the blank control group, Rg3 significantly reduced the invasion of BGC-823 cells, while IGF-1 and IGF-1+Rg3 significantly promoted the invasion of BGC-823 cells (all P<0.05);Flow cytometry showed that compared with the blank control group, Rg3 significantly promoted the apoptosis of BGC-823 cells, while IGF-1 and IGF-1+Rg3 significantly inhibited the apoptosis of BGC-823 cells (all P<0.05). Conclusion: Ginsenoside Rg3 inhibits the expression of CaM by blocking PI3K/AKT signaling pathway, thereby promoting the apoptosis of gastric cancer BGC-823 cells.