PI3 K/AKT/mTOR信号通路与肺癌TKI耐药性及放疗抵抗性

肺癌的发病率及病死率一直居高不下，目前针对表皮生长因子受体以及抗血管内皮生长因子受体等的靶向治疗药物已成为临床一线用药，并辅助以放疗、手术治疗等。但是，临床发现肺癌细胞容易对药物产生耐药性，对放疗的敏感性也容易下降。研究发现 PI3K/AKT/mTOR 通路广泛存在于多种癌症细胞中，在细胞生长、增殖、血管生成等过程中起重要调节作用。不少研究学者发现，该通路的激活与肺癌细胞对表皮生长因子受体-酪氨酸激酶抑制剂的耐药性和放疗的抵抗性呈现正相关。PI3K/AKT抑制剂或 mTOR抑制剂均可逆转肺癌细胞的耐药性及放疗抵抗性，并有望成为治疗肺癌的新型抗癌药物。本文就近几年该信号通路有关的报道进行总结。

Relationship of PI3K/AKT/mTOR pathway with TKI drug and radiation resistance

Lung cancer is the leading cause of cancer-related mortality worldwide.Currently, epidermal growth factor receptor and anti-vascular endothelial growth factor receptor have become first-line clinical application.But the lung carcinoma can tend to be resistant of targeted therapies and radiation. The researches have found that PI3K/AKT/mTOR pathway widely exists in many kinds of cancer cells and it plays an important role in the process of cell growth,proliferation and angiogenesis.We find that the pathways is closely associated with tyrosine kinase inhibitor and radiation resistance.The PI3K/AKT inhibitor could reverse the drug resistance of epidermal growth factor receptor-tyrosine kinase inhibitor. The same as the mTOR inhibitor for the radiation sensitivity.These findings may provide basic evidence for PI3K/AKT inhibitor and mTOR inhibitor applied in the treatment of lung cancer.