Effects Of PI3K/NF-κB Inhibitor On Gastric Cancer SGC7901 Cells

Objective: To study the mechasim of autophagy and apoptosis on SGC7901 gastric cancer cells in blocking PI3K/NF-κB pathway SGC7901.Methods: The MTT assay was used to determine the cytotoxic effects of LY294002 or SN50. Cell cycle distribution was analyzed using flow cytometry and apoptosis was assessed using flow cytometry analysis after staining DNA with propidium iodide. Mitochondrial membrane potential was measured using the fluorescent probe JC-1. Molecular mechanism was determined using Western blotting analysis. The expression of autophagy was monitored with monodansylcadaverin (MDC) staining,LC3 immunofluorescence and Transmission Electron Microscope (TEM) after LY294002 or SN50 treatment.Results: LY294002 inhibited the growth of cells, induced mitochondrial dysfunction by upregulating the level of autophagy, and promoted apoptosis of SGC7901 cells. The results proved that LY294002 induced apoptosis in SGC7901 cells. It indicated that the inhibitor of PI3K signal transduction promoted apoptosis by increasing the level of autophagy, upregulated the expression of LC3 and Beclin1 and increased the expression of p53 and PUMA. The inhibitor of NF-κB p65 nuclear translocation inhibited the growth of cells, induced mitochondrial dysfunction by activating the autophagy and promoted autophagic cell death. It indicated that the inhibitor of NF-κB p65, activated the expression of autophagy specific protein LC3 and autophagy-related protein Beclin1; enhanced the expression of p53 and PUMA.Conclusion: The inhibitor of PI3K upregulated autophagy and promoted cell apoptosis in gastric cancer SGC7901 cell line; the inhibitor of NF-κB p65 nuclear translocation activated autophagy and induced autophagic cell death in gastric cancer SGC7901 cell line.