Metabolic alterations accompanying oncogene-induced senescence.
Metabolic alterations accompanying oncogene-induced senescence.
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DOI：
10.4161/23723548.2014.963481
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发表时间：
2014-07
影响因子：
2.1
通讯作者：
Zhang R
中科院分区：
文献类型：
--
作者：
Aird KM;Zhang R
衰老被定义为一种稳定的细胞生长停滞。癌基因诱导的衰老（OIS）发生在正常的原代人细胞中，在没有其他协同致癌刺激的情况下，癌基因被激活。因此，OIS被认为是一种真正的体内肿瘤抑制机制。事实上，克服ois相关的稳定细胞生长阻滞可导致肿瘤发生。虽然经历OIS的细胞不会复制DNA，但它们仍保持代谢活性。最近的一些研究报道了OIS期间细胞代谢的显著变化，包括核苷酸、葡萄糖、线粒体代谢和自噬的改变。这些改变可能是稳定的衰老相关细胞生长停滞所必需的，克服这些代谢变化可能导致肿瘤发生。这篇综述强调了目前已知的OIS期间细胞代谢的变化，以及OIS相关代谢变化在细胞转化和癌症治疗策略发展中的意义。
Senescence is defined as a stable cell growth arrest. Oncogene-induced senescence (OIS) occurs in normal primary human cells after activation of an oncogene in the absence of other cooperating oncogenic stimuli. OIS is therefore considered a bona fide tumor suppression mechanism in vivo. Indeed, overcoming OIS-associated stable cell growth arrest can lead to tumorigenesis. Although cells that have undergone OIS do not replicate their DNA, they remain metabolically active. A number of recent studies report significant changes in cellular metabolism during OIS, including alterations in nucleotide, glucose, and mitochondrial metabolism and autophagy. These alterations may be necessary for stable senescence-associated cell growth arrest, and overcoming these shifts in metabolism may lead to tumorigenesis. This review highlights what is currently known about alterations in cellular metabolism during OIS and the implication of OIS-associated metabolic changes in cellular transformation and the development of cancer therapeutic strategies.