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Redox signalling in anchorage-dependent cell growth

机译：氧化还原信号在锚固依赖性细胞生长中

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Current data have provided new perspectives concerning the regulation of non-transformed cell proliferation in response to both soluble growth factors and to adhesive cues. Non-transformed cells are anchorage dependent for the execution of the mitotic program and cannot avoid the concomitant signals starting from mitogenic molecules, as growth factors, and adhesive agents belonging to extracellular matrix. Reactive oxygen species play a key role during both growth factor and integrin receptor signalling and these second messengers are recognised to have a synergistic function for anchorage-dependent growth signalling. Redox regulated proteins include protein tyrosine phosphatases and protein tyrosine kinases, although with opposite regulation of their enzymatic activity, and cytoskeletal proteins as beta-actin. In this review we support a role of ROS as key second messengers granting a proper executed mitosis for anchorage-dependent cells, through redox regulation of several downstream targets. Deregulation of these redox pathways may help to guide transformed cells to elude the native apoptotic response to abolishment of signals started by cell/ECM contact, sustaining ectopic anchorage-independent cancer cell growth. (c) 2006 Elsevier Inc. All rights reserved.
机译：当前的数据提供了关于响应于可溶性生长因子和粘附线索而调节非转化细胞增殖的新观点。非转化细胞在有丝分裂程序的执行过程中依赖于锚定，并且不能避免从有丝分裂分子（作为生长因子）和属于细胞外基质的黏附剂开始的伴随信号。活性氧在生长因子和整联蛋白受体信号传导中均起关键作用，并且这些第二信使被认为对锚定依赖性生长信号传导具有协同作用。氧化还原调节的蛋白包括蛋白酪氨酸磷酸酶和蛋白酪氨酸激酶，尽管它们的酶活性具有相反的调节作用，而细胞骨架蛋白则为β-肌动蛋白。在这篇综述中，我们支持ROS作为关键的第二信使的作用，它通过对多个下游靶标的氧化还原调节，为锚定依赖性细胞提供了适当的有丝分裂。这些氧化还原途径的失调可能有助于引导转化细胞逃避对细胞/ ECM接触开始的信号消失的天然凋亡反应，从而维持异位锚定非依赖性癌细胞的生长。 （c）2006 Elsevier Inc.保留所有权利。

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