API-2靶向抑制P13K／Akt信号通路干预胃癌细胞生长的研究

目的研究蛋白激酶B抑制剂-2（API-2）靶向抑制P13K／Akt信号通路中Akt位点，从而对胃癌细胞生长的影响。方法使用API-2处理人胃癌细胞株SGC7901。MTT法检测0，2，4，6，8μmol／LAPI-2作用不同时间对细胞增殖的影响；荧光染料A0／EB染色观察不同浓度API-2作用24h后细胞凋亡情况；流式细胞仪检测细胞周期变化；Westernblot法检测P—AKT蛋白以及下游蛋白NF-κB表达情况。结果API-2可抑制SGC7901细胞的增殖，并呈浓度和时间依赖性；不同浓度API-2作用24h后，对细胞的部分周期有明显的影响，也可直接导致肿瘤细胞凋亡、坏死，并且p-AKT蛋白及下游蛋白NF-κB表达均减少。结论API-2有效地抑制P13K／Akt信号通路中Akt位点，影响SGC7901细胞的周期．减少NF-κB的表达，具有增殖抑制及诱导凋亡作用。

Effects of Selective Inhibition by API-2 on the Growth of Gastric Cancer Cells

Objective To study the effect of the inhibition of Akt by API-2 in PI3K/Akt signaling pathway on the growth of gastric cancer cells. Methods SGC7901 cells were treated with API-2. The effect of API-2 （0,2,4,6,8 μmol/L） on their proliferation was observed with MTT assay. Cell apoptosis after treated with API-2 for 24 h was observed by AO/EB double staining for fluorescence microscopy. Cell cycle was analyzed by flow cytometry （FCM）. The expression of p-AKT and NF-κB was detected by Western blot. Results API-2 （0,2,4,6,8 μmol/L） significantly inhibited the proliferation of SGC7901 cells in dose-and time-dependent manner. When treated with different densities of API-2 for 24 h, parts of the cell cycle of SGC7901 cells were obviously blocked. Apoptosis and necrosis of the tumor ceils were increased while p-AKT and NF-κB expression was decreased. Conclusion API-2 can inhibit proliferation and induce apoptosis of SGC7901 cells by effectively inhibiting Akt in PI3K/Akt signaling pathway, affecting cell cycle distributions of the cells, and greatly reducing the expression of NF-κB.