API2靶向抑制PI3KAkt信号通路干预胃癌细胞生长的研究.docxVIP

API 2靶向抑制PI3K/Akt信号通路干预胃癌细胞生长的研究 【摘要】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SGC7901o IVTT法检测 0,2, 4, 6, 8 p n?l/L API 2作用不同时间对细胞增殖的影响;荧光 染料ACY EB染色观察不同浓度API 2作用24 h后细胞凋亡情况； 流式细胞仪检测细胞周期变化；Astern bl ot法检测p AKT蛋白 以及下游蛋白M k B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24 h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M k B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hF K B的表达，具有增殖抑制及诱导凋亡作用。 【关键词】胃肿瘤;蛋白酶抑制药;1磷脂酰肌醇3 激酶;蛋白 质丝氨酸苏氨酸激酶;M K B;信号传导;细胞凋亡;肿瘤细胞，培养 的 ABSTRACT: Cbj ecti ve To study the effect of the i nhi bi ti on of Akt by API 2 i n PI3K/Akt si gnal i ng pathvvay on the grovlhof gastri c cancer cel I s? l\^t hods SGC7901 cel I s v\ere treated w th API 2. The effect of API 2 (0 , 2,4,6 , 8 p ikdI /L) on thei r prol i ferati on\Aas observed w th MT assa y. Cel I apopt os i s after treated w th API 2 for 24 h v\as observed by ACYEBdoubl e stai ni ng for fl uorescence nncroscopy. Cel I eye I e v\as anal yzed by fl ow cytorietry ( FCM ? The expressi on of p AKT and hF Apo pt os ik B v\as detected by Vastern bl ot. Resul ts API 2 (0 , 2 z 4 , 6,8 p nrol / L) si gni f i cant I y i nhi bi ted the prol i ferati on of SGC7901 cel I s i n dose and ti rre dependent nanner. Wien treated w th di ff er ent densi ti es of API 2 for 24 h, parts of t he cel I eye I e of SGC7901 cel I s \Aere obvi ousl y bl ocked. Apo pt os i s and necrosi s of the tun?r cel I s v\ere i ncreased v\hi I e p AKT and hF k B expressi on v\as decreased. Concl usi on API 2 can i nhi bi t prol i ferati on and i nduce apopt os i s of SGC7901 cel I s by eff ecti vel y in hi bi t i ng Akt i n PI3K/Akt si gnal i ng pathv\ay, affect in g cel I cycl e di stri but i ons of the cel I s, and great I y reduci ng the expressi on of hF k B. i nhi bi tors; 1seri netransducti on;KEY V€RDS: storrach neopl as ns; protease i nhi bi tors; 1 seri ne transducti on; phos phat i dy lin osi tol 3 ki nase; protei n threoni ne ki nases; hF kappa B; si gnal apopt osi s;