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磷脂肌醇(PI3K)-蛋白激酶B(PKB,Akt)-雷帕霉素靶体蛋白(mTOR)通路抑制剂耐药现象的出现,与其上下游相关联的其他癌蛋白信号通路的反馈机制密切相关。目前已经报道的有关PI3K-Akt-mTOR通路抑制剂耐药机制,基本上可以分为与FOXO和激素受体相关,依赖于MYC,依赖于β-catenin,依赖于JAK/STAT通路,依赖于MAPK通路,及与AXL相关的耐药机制。PI3K-Akt-mTOR通路抑制剂的耐药,极大地影响了该类小分子靶向药物在临床上的使用,通过对其耐药性产生的机制进行探讨和总结,为临床上和其他药物联用克服该类靶向药物耐药提供策略。
The emergence of resistance to phosphorylated inositol (PI3K) - protein kinase B (PKB, Akt) - rapamycin pathway protein (mTOR) pathway inhibitor and the feedback mechanism of other oncoprotein signaling pathways closely related to its upstream and downstream Related. It has been reported that the mechanism of PI3K-Akt-mTOR pathway inhibitor resistance can basically be divided into FOXO and hormone receptor dependent, MYC dependent, β-catenin dependent, JAK / STAT pathway dependent MAPK Pathways, and resistance mechanisms associated with AXL. The resistance of PI3K-Akt-mTOR pathway inhibitor has greatly affected the clinical use of this kind of small molecule targeted drugs. Through exploring and summarizing the mechanism of its drug resistance, Strategies to overcome this type of targeted drug resistance are provided.