Under normal conditions, basal levels of wild-type p53 promote mitochondrial function through multiple mechanisms. Remarkably, some missense mutations of p53, in contrast to the null state, can result in the retention of its metabolic activities. These effects are particularly prominent in the mitochondria and demonstrate a functional role for mutant p53 in cancer metabolism. This review summarizes accumulating data on the mechanisms by which p53 missense mutations can regulate mitochondrial metabolism and promote the viability and survival of both normal and cancer cells, thus acting as a double edged sword for the host. Greater understanding of these mechanisms may provide insights for developing new treatment or preventive strategies against cancer.

中文翻译：

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TP53突变，线粒体和癌症。

在正常条件下，野生型p53的基础水平通过多种机制促进线粒体功能。值得注意的是，与无效状态相比，p53的一些错义突变可以导致其代谢活性的保持。这些作用在线粒体中尤为突出，并证明突变体p53在癌症代谢中具有功能性作用。这篇综述总结了有关p53错义突变可调节线粒体代谢并促进正常细胞和癌细胞存活和存活的机制的数据，因此可作为宿主的双刃剑。对这些机制的更多理解可能为开发针对癌症的新疗法或预防策略提供见识。