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Suppression of c-Myc-induced apoptosis by Ras signalling through PI(3)K and PKB

机译：通过PI（3）K和PKB的Ras信号抑制c-Myc诱导的细胞凋亡

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摘要

The viability of vertebrate cells depends on survival factors which activate signal transduction pathways that suppress apoptosis. Defects in anti-apoptotic signalling pathways are implicated in many pathologies including cancer, in which apoptosis induced by deregulated oncogenes must be forestalled for a tumour to become established. Phosphatidylinositol-3-kinase (PI(3)K) is involved in the intracellular signal transduction of many receptors and has been implicated in the transduction of survival signals in neuronal cells. We therefore examined the role of PI(3)K, its upstream effector Ras, and its putative downstream protein kinase effectors PKB/Akt and p70S6K (ref. 5) in the modulation of apoptosis induced in fibroblasts by the oncoprotein c-Myc. Here we show that Ras activation of PI(3)K suppresses c-Myc-induced apoptosis through the activation of PKB/Akt but not p70S6K. However, we also found that Ras is an effective promoter of apoptosis, through the Raf pathway. Thus Ras activates contradictory intracellular pathways that modulate cell viability. Induction of apoptosis by Ras may be an important factor in limiting the expansion of somatic cells that sustain oncogenic ras mutations.
机译：脊椎动物细胞的生存能力取决于存活因子，该因子激活抑制细胞凋亡的信号转导途径。抗凋亡信号通路的缺陷与包括癌症在内的许多疾病有关，其中必须阻止癌基因失控诱导的凋亡，才能使肿瘤得以建立。磷脂酰肌醇-3-激酶（PI（3）K）参与许多受体的细胞内信号转导，并参与神经元细胞中生存信号的转导。因此，我们检查了PI（3）K，其上游效应子Ras和其假定的下游蛋白激酶效应子PKB / Akt和p70S6K（参考文献5）在癌蛋白c-Myc诱导的成纤维细胞凋亡调控中的作用。在这里，我们显示Ras的PI（3）K激活通过激活PKB / Akt而不是p70S6K抑制c-Myc诱导的凋亡。但是，我们还发现Ras通过Raf途径是凋亡的有效启动子。因此，Ras激活了调节细胞活力的矛盾细胞内途径。 Ras诱导细胞凋亡可能是限制维持致癌ras突变的体细胞扩增的重要因素。

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