The Selective Inhibition Of API-2 On The Growth Of Gastric Cancer Cells

BACKGROUND&OBJECTIVE Many studies have showed that PI3K/Akt signaling pathway and its downstream effector molecule nuclear factor-kappa B play important roles in cell proliferation, apoptosis and oncogenesis. However, the expression of p-AKT and NF-ΚB in gastric cancer cells has rarely been reported. The study aims at looking for a new target for anticancer therapy, based on the relationship between Akt and NF-κB in the expression of human gastric cancer cells when Akt is inhibited by API-2, a small molecule Akt signaling pathway inhibitor, highly selective for Akt.METHODS MTT assay was used to observe the effect of API-2 (0, 2, 4, 6, 8μmol/L) on proliferation of SGC7901 cells. Cell apoptosis was observed by AO/EB double staining for fluorescence microscopy when treated with API-2 for 24h. Cell cycle was analyzed by flow cytometry (FCM). The expression of p-AKT and NF-κB was detected by Western blot.RESULTS API-2 (0, 2, 4, 6, 8μmol/L) significantly inhibited the proliferation of SGC7901 cells in dose- and time-dependent manners. When treated with different densities of API-2 for 24h, parts of the cell cycle of SGC7901 cells were obviously blocked. And apoptosis and necrosis of the tumor cells were increased, meanwhile, p-AKT and NF-κB expression were decreased.CONCLUSION By effectively inhibiting Akt in PI3K/Akt signaling pathway, affecting cell cycle distributions of the tumor cells, greatly reducing expression of NF-κB, API-2 inhibits proliferation and induce apoptosis of SGC7901 cells.