Improving Chemotherapeutic Effect of Lung Adenocarcinoma by Inhibiting PI3K/ Akt Sig2 nal Pathway

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.