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目的研究蛋白激酶B抑制剂-2(API-2)靶向抑制PI3K/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AO/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;Western blot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PI3K/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。
Objective To investigate the effect of protein kinase B inhibitor-2 (API-2) on the inhibition of Akt signaling in PI3K / Akt signaling pathway and its effect on the growth of gastric cancer cells. Methods Human gastric cancer cell line SGC7901 was treated with API-2. The effects of 0, 2, 4, 6 and 8μmol / L API-2 on cell proliferation were detected by MTT assay. Apoptosis of cells treated with different concentrations of API-2 was observed by fluorescent dye AO / EB staining. Flow cytometry Cell cycle changes were detected by Western blot. The expression of p-AKT protein and NF-κB protein was detected by Western blot. Results API-2 inhibited the proliferation of SGC7901 cells in a concentration- and time-dependent manner. After treated with different concentrations of API-2 for 24 h, API-2 had a significant effect on the cell cycle and also directly induced the apoptosis and necrosis of tumor cells p-AKT protein and downstream protein NF-κB expression were reduced. Conclusions API-2 effectively inhibits the Akt signaling pathway in PI3K / Akt signaling pathway, affects the cycle of SGC7901 cells, decreases the expression of NF-κB, and has the effects of inhibiting proliferation and inducing apoptosis.