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Akt-dependent and -independent mechanisms of mTOR regulation in cancer

机译：癌症中mTOR调节的Akt依赖性和非依赖性机制

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The protein kinase mTOR (mammalian target of rapamycin) is a critical regulator of cellular metabolism, growth, and proliferation. These processes contribute to tumor formation, and many cancers are characterized by aberrant activation of mTOR. Although activating mutations in mTOR itself have not been identified, deregulation of upstream components that regulate mTOR are prevalent in cancer. The prototypic mechanism of mTOR regulation in cells is through activation of the PI3K/Akt pathway, but mTOR receives input from multiple signaling pathways. This review will discuss Akt-dependent and -independent mechanisms of mTOR regulation in response to mitogenic signals, as well as its regulation in response to energy and nutrient-sensing pathways. Preclinical and clinical studies have demonstrated that tumors bearing genetic alterations that activate mTOR are sensitive to pharmacologic inhibition of mTOR. Elucidation of novel pathways that regulate mTOR may help identify predictive factors for sensitivity to mTOR inhibitors, and could provide new therapeutic targets for inhibiting the mTOR pathway in cancer. This review will also highlight pharmacologic approaches that inhibit mTOR via activation of the AMP-activated protein kinase (AMPK), an important inhibitor of the mTOR pathway and an emerging target in cancer. Published by Elsevier Inc.
机译：蛋白激酶mTOR（雷帕霉素的哺乳动物靶标）是细胞代谢，生长和增殖的关键调节剂。这些过程有助于肿瘤形成，并且许多癌症的特征在于mTOR的异常激活。尽管尚未确定mTOR本身的激活突变，但调节mTOR的上游成分的失控在癌症中很普遍。细胞中mTOR调控的原型机制是通过激活PI3K / Akt途径，但mTOR从多个信号途径接收输入。这篇综述将讨论对有丝分裂信号响应的mTOR调节的Akt依赖性和非依赖性机制，以及对能量和养分感应途径的响应的调节。临床前和临床研究表明，具有激活mTOR的基因改变的肿瘤对mTOR的药理抑制敏感。阐明调节mTOR的新途径可能有助于确定对mTOR抑制剂敏感性的预测因素，并可能为抑制癌症中的mTOR途径提供新的治疗靶点。这篇综述还将重点介绍通过激活AMP激活的蛋白激酶（AMPK）来抑制mTOR的药理学方法，AMPK是mTOR途径的重要抑制剂，也是癌症的新兴靶标。由Elsevier Inc.发布

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