PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers.

PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers.
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PI3K/AKT通路是调控肿瘤多药耐药的关键环节。

DOI:
10.1038/s41419-020-02998-6
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发表时间:
2020-09-24
影响因子:
9
通讯作者:
Liu Y
Liu Y
中科院分区:
生物学1区
文献类型:
--
作者:
Liu R;Chen Y;Liu G;Li C;Song Y;Cao Z;Li W;Hu J;Lu C;Liu Y

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多药耐药(MDR)是肿瘤化疗失败的主要原因。磷脂酰肌醇3-激酶(PI 3 K)是一种传递细胞内信号级联并调节多种细胞过程的脂质激酶。PI 3 K被认为是癌症治疗中化学抗性的重要原因。蛋白激酶B(AKT)也是PI 3 K信号传导的重要下游效应物,并且其调节若干途径,包括抑制细胞凋亡、刺激细胞生长和调节细胞代谢。本文综述了PI 3 K/AKT的异常激活作为调节MDR的关键环节。我们总结了与PI 3 K/AKT途径相关的许多主要靶点的调节,该途径与MDR进一步相关,包括细胞凋亡相关蛋白的表达、ABC转运和糖原合成酶激酶-3 β(GSK-3β)、与核因子kappa β(NF-κ)的协同作用。B)和哺乳动物雷帕霉素靶点(mTOR),以及糖酵解的调节。
Multidrug resistance (MDR) is the dominant challenge in the failure of chemotherapy in cancers. Phosphatidylinositol 3-kinase (PI3K) is a lipid kinase that spreads intracellular signal cascades and regulates a variety of cellular processes. PI3Ks are considered significant causes of chemoresistance in cancer therapy. Protein kinase B (AKT) is also a significant downstream effecter of PI3K signaling, and it modulates several pathways, including inhibition of apoptosis, stimulation of cell growth, and modulation of cellular metabolism. This review highlights the aberrant activation of PI3K/AKT as a key link that modulates MDR. We summarize the regulation of numerous major targets correlated with the PI3K/AKT pathway, which is further related to MDR, including the expression of apoptosis-related protein, ABC transport and glycogen synthase kinase-3 beta (GSK-3β), synergism with nuclear factor kappa beta (NF-κB) and mammalian target of rapamycin (mTOR), and the regulation of glycolysis.
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