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首页> 外文期刊>Cell cycle >Inactivation of p53 signaling by p73 or PTEN ablation results in a transformed phenotype that remains susceptible to nutlin-3 mediated apoptosis.
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Inactivation of p53 signaling by p73 or PTEN ablation results in a transformed phenotype that remains susceptible to nutlin-3 mediated apoptosis.

机译：通过p73或PTEN消融使p53信号失活导致转化的表型仍然对nutlin-3介导的凋亡敏感。

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摘要

The p53 signaling pathway is frequently disrupted in carcinogenesis. However, roughly 50% of all cancers express wild-type p53 and have alterations in accessory signaling components required for p53 activity. Using the well described E1A/RAS transformation model, in which p53 activity must be suppressed for transformation, we show here that p53 is inactive and unable to suppress transformation following ablation of p73 or PTE N. However, despite the transformed phenotype conferred by p53 inactivation following p73 or PTE N loss, p53 could be fully activated by Nutlin-3, resulting in efficient caspase-mediated apoptosis. Our novel and unexpected finding provides important information regarding the efficacy of Nutlin-3 and indicates that patients with tumors deficient in p53 function due to p73 or PTE N loss may benefit from Nutlin-3 treatment.
机译：p53信号通路在致癌作用中经常被破坏。但是，所有癌症中大约有50％表达野生型p53，并具有p53活性所需的辅助信号成分的改变。使用众所周知的E1A / RAS转化模型，其中必须抑制p53活性才能进行转化，我们在这里显示p53处于无活性，并且不能消融p73或PTE N后的转化。但是，尽管p53失活赋予了转化表型在p73或PTE N缺失后，p53可以被Nutlin-3完全激活，从而导致有效的caspase介导的细胞凋亡。我们新颖而出乎意料的发现提供了有关Nutlin-3功效的重要信息，并表明由于p73或PTE N缺失而导致p53功能缺陷的肿瘤患者可能会受益于Nutlin-3治疗。

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