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.