抑制PI3 K/ Akt 通路提高肺腺癌细胞化疗的 效果
Improving Chemotherapeutic Effect of Lung Adenocarcinoma by Inhibiting PI3K/ Akt Sig2 nal Pathway
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摘要: 目的 探讨PI3 K/ Akt 信号转导通路抑制剂L Y294002 对肺腺癌细胞株A549 及裸鼠移植瘤化疗的增敏作用。方法 采用MTT 法及流式细胞仪检测L Y294002 、紫杉醇、L Y294002 联合紫杉醇对A549 细胞增殖及凋亡的影响;通过裸鼠移植瘤模型检测L Y294002 、紫杉醇、L Y294002 联合紫杉醇对A549 细胞成瘤性的影响。结果 L Y294002 可增强紫杉醇对A549 细胞的抑制作用,并且可提高其凋亡率。裸鼠移植瘤实验显示,L Y294002 与紫杉醇均可抑制移植瘤的生长,联用后抑瘤率增加。结论 L Y294002 可增强紫杉醇对A549 细胞、裸鼠移植瘤的化疗的敏感性,抑制PI3 K/ Akt 信号转导通路可提高肺腺癌化疗的效果。Abstract: Objective To explore the effect s of specific inhibitor L Y294002 of the PI3 K/ Akt signaling pathway in enhancing sensitivity to chemotherapeutic agent of lung adenocarcinoma cell line A549 and im2 planted tumor of nude mice. Methods The effect s of L Y294002 、paclitaxel liposome、L Y294002 com2 bined with paclitaxel liposome on proliferation and apoptosis of human lung cancer cell line A549 were e2 valuated by MTT reduction assay and flow cytomet ry respectively ; and the effect s of that on neoplasia were verified by modeling subcutaneous implanted tumor of nude mice. Results L Y294002 could in2 crease the inhibitory effect of the paclitaxel liposome and increase the apoptosis ratio on cell line A549 in vit ro. L Y294002 and paclitaxel liposome could inhibit the growth of subcutaneous implanted tumor of nude mice and the inhibitory rate of L Y294002 combined with paclitaxel liposome was higher significantly than that of L Y294002 and paclitaxel liposome alone ( P < 0. 01) . Conclusion The L Y294002 can en2 hance sensitivity to chemotherapeutic agent of lung adenocarcinoma cell line A549 and subcutaneous im2 planted tumor of nude mice. Inhibiting the PI3 K/ Akt signaling pathway can increase the chemotherapeu2 tic sensitivity of lung adenocarcinoma.