CA916798基因通过PI3K/AKT/mTOR通路参与顺铂耐药的机制分析

摘要：目的观察阻断PI3K/AKT/mTOR通路对人肺腺癌细胞A549 及多药耐药人肺腺癌细胞A549/CDDP内CA916798 基因
mRNA表达的影响。方法以雷帕霉素、LY294002分别作用于人肺腺癌细胞A549和多药耐药人肺腺癌细胞A549/CDDP，检测
顺铂作用后细胞生长及增殖情况，RT-PCR 检测CA916798 基因mRNA表达水平。结果以雷帕霉素和LY294002 分别阻断
A549、A549/CDDP细胞的PI3K/AKT/mTOR通路后，细胞对于顺铂的耐药性均显著下降（P<0.05），CA916798基因的表达均显
著下调（P<0.05）。结论CA916798基因位于PI3K/AKT/mTOR通路下游，可能是CA916798诱导肺癌顺铂耐药的机制之一。

CA916798 gene participates in cisplatin resistance of human lung adenocarcinoma A549 cells through PI3K/AKT/mTOR pathway

Objective To observe the changes of CA916798 gene expression in human lung adenocarcinoma cell A549 and the multidrug-resistant cell line A549/CDDP after blocking the PI3K/AKT/mTOR pathway.Methods Human lung adenocarcinoma cell lines A549 and A549/CDDP were treated with rapamycin and LY294002,and the cell growth changes in response to subsequent cisplatin treatment was observed;RT-PCR was performed to detect CA916798 mRNA expression in the treated cells.Results Blocking PI3K/AKT/mTOR pathway with rapamycin and LY294002 significantly reduced drug resistance of both A549 and A549/CDDP cells to cisplatin and obviously decreased the expression of CA916798 gene mRNA(P<0.05).Conclusion CA9167981 gene is located downstream of the PI3K/AKT/mTOR pathway,which might be one of the mechanisms of CA916798 to cause cisplatin resistance in the tumor cells.