RAS 和 RHO 信号通路在细胞转化、运动和收缩中的交叉点,Genes

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RAS 和 RHO 信号通路在细胞转化、运动和收缩中的交叉点
Genes ( IF 2.8 ) Pub Date : 2021-05-27 , DOI: 10.3390/genes12060819
Olga Soriano ₁ , Marta Alcón-Pérez ₂ , Miguel Vicente-Manzanares ₁ , Esther Castellano ₂

Affiliation

Ras 和 Rho 蛋白是 GTP 调节的分子开关，可控制真核细胞中的多个信号通路。Ras 是最早发现的致癌基因之一，它似乎在多种形式的人类癌症中发生了突变。它主要分别通过MAPK途径和PI3K/AKT途径促进增殖和存活。然而，靠近质膜的无数激活或抑制 Ras 的蛋白质使其成为许多明显不相关的途径的主要调节剂。另一方面，Rho 本身具有弱致癌性，但它严格调节微丝动力学；即肌动蛋白聚合、分解和收缩。聚合主要由 Arp2/3 复合物和 formins 驱动，而收缩取决于肌球蛋白微丝组装和活性。这两条路径在许多点相交：从 Rho 激活剂的 Ras 依赖性触发（其中一些通过 PI3K 起作用）到由肌动球蛋白作用驱动的机械反馈。在这里，我们描述了 Ras 和 Rho 通路之间的主要连接点，因为它们协同驱动致癌转化。我们强调以 Rho 依赖性方式驱动由 Ras 驱动的肌动球蛋白收缩的生化串扰。我们还描述了机械反馈的可能途径，肌球蛋白 II 激活可以通过这些途径控制 Ras/Rho 激活。我们强调以 Rho 依赖性方式驱动由 Ras 驱动的肌动球蛋白收缩的生化串扰。我们还描述了机械反馈的可能途径，肌球蛋白 II 激活可以通过这些途径控制 Ras/Rho 激活。我们强调以 Rho 依赖性方式驱动由 Ras 驱动的肌动球蛋白收缩的生化串扰。我们还描述了机械反馈的可能途径，肌球蛋白 II 激活可以通过这些途径控制 Ras/Rho 激活。

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The Crossroads between RAS and RHO Signaling Pathways in Cellular Transformation, Motility and Contraction

Ras and Rho proteins are GTP-regulated molecular switches that control multiple signaling pathways in eukaryotic cells. Ras was among the first identified oncogenes, and it appears mutated in many forms of human cancer. It mainly promotes proliferation and survival through the MAPK pathway and the PI3K/AKT pathways, respectively. However, the myriad proteins close to the plasma membrane that activate or inhibit Ras make it a major regulator of many apparently unrelated pathways. On the other hand, Rho is weakly oncogenic by itself, but it critically regulates microfilament dynamics; that is, actin polymerization, disassembly and contraction. Polymerization is driven mainly by the Arp2/3 complex and formins, whereas contraction depends on myosin mini-filament assembly and activity. These two pathways intersect at numerous points: from Ras-dependent triggering of Rho activators, some of which act through PI3K, to mechanical feedback driven by actomyosin action. Here, we describe the main points of connection between the Ras and Rho pathways as they coordinately drive oncogenic transformation. We emphasize the biochemical crosstalk that drives actomyosin contraction driven by Ras in a Rho-dependent manner. We also describe possible routes of mechanical feedback through which myosin II activation may control Ras/Rho activation.

更新日期：2021-05-27

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