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首页> 美国卫生研究院文献>Cells Tissues Organs >Emergence of the Phosphoinositide 3-Kinase-Akt-Mammalian Target of Rapamycin Axis in Transforming Growth Factor-β-Induced Epithelial-Mesenchymal Transition
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Emergence of the Phosphoinositide 3-Kinase-Akt-Mammalian Target of Rapamycin Axis in Transforming Growth Factor-β-Induced Epithelial-Mesenchymal Transition

机译：雷帕霉素轴的磷酸肌醇3-激酶-Akt-哺乳动物靶标在转化生长因子-β-诱导的上皮-间质转化中的出现

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During development and in pathological contexts such as fibrosis and cancer progression, epithelial cells can initiate a complex transcriptional reprogramming, accompanied by dramatic morphological changes, in a process named ‘epithelial-mesenchymal transition’ (EMT). In this transition, epithelial cells lose their epithelial characteristics to acquire mesenchymal properties and increased motile and invasive behavior. Transforming growth factor-β (TGF-β) has emerged as a major inducer of EMT through activation of downstream signaling pathways, including Smad and non-Smad signaling pathways. Among the non-Smad pathways, increasing evidence is emerging that the phosphoinositide 3-kinase-Akt-mammalian target of rapamycin axis plays a major role in TGF-β-induced EMT, notably through the regulation of translation and cell invasion. Pharmacological inhibitors of the phosphoinositide 3-kinase-Akt-mammalian target of rapamycin pathway may therefore represent an opportunity to selectively target essential aspects of TGF-β-induced EMT and provide an approach to prevent cancer cell dissemination toward metastasis, without the need to fully inactivate TGF-β signaling.
机译：在发育过程中以及在诸如纤维化和癌症进展之类的病理情况下，上皮细胞可以在称为“上皮-间质转化”（EMT）的过程中启动复杂的转录重编程，并伴随着剧烈的形态变化。在这种转变中，上皮细胞丧失其上皮特性，从而获得了间充质特性并增加了运动和侵袭行为。转化生长因子-β（TGF-β）已通过激活下游信号通路（包括Smad和非Smad信号通路）而成为EMT的主要诱因。在非Smad途径中，越来越多的证据表明雷帕霉素轴的磷酸肌醇3-激酶-Akt-哺乳动物靶标在TGF-β诱导的EMT中起主要作用，特别是通过调节翻译和细胞侵袭。因此，雷帕霉素途径的磷酸肌醇3-激酶-Akt-哺乳动物靶标的药理抑制剂可能代表有机会选择性地靶向TGF-β诱导的EMT的基本方面，并提供一种防止癌细胞向转移扩散的方法，而无需完全使TGF-β信号失活。

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