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首页> 外文期刊>Cell cycle >Is cancer a metabolic rebellion against host aging? In the quest for immortality, tumor cells try to save themselves by boosting mitochondrial metabolism
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Is cancer a metabolic rebellion against host aging? In the quest for immortality, tumor cells try to save themselves by boosting mitochondrial metabolism

机译：癌症是抵抗宿主衰老的新陈代谢吗？在寻求永生的过程中，肿瘤细胞试图通过促进线粒体代谢来拯救自己

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Aging drives large systemic reductions in oxidative mitochondrial function, shifting the entire body metabolically toward aerobic glycolysis, a.k.a, the Warburg effect. Aging is also one of the most significant risk factors for the development of human cancers, including breast tumors. How are these two findings connected? One simplistic idea is that cancer cells rebel against the aging process by increasing their capacity for oxidative mitochondrial metabolism (OXPHOS). Then, local and systemic aerobic glycolysis in the aging host would provide energy-rich mitochondrial fuels (such as L-lactate and ketones) to directly "fuel" tumor cell growth and metastasis. This would establish a type of parasite-host relationship or "two-compartment tumor metabolism," with glycolytic/oxidative metabolic-coupling. The cancer cells ("the seeds") would flourish in this nutrient-rich microenvironment ("the soil"), which has been fertilized by host aging. In this scenario, cancer cells are only trying to save themselves from the consequences of aging, by engineering a metabolic mutiny, through the amplification of mitochondrial metabolism. We discuss the recent findings of Drs. Ron DePinho (MD Anderson) and Craig Thomspson (Sloan-Kettering) that are also consistent with this new hypothesis, linking cancer progression with metabolic aging. Using data mining and bioinformatics approaches, we also provide key evidence of a role for PGC1a/ NRF1 signaling in the pathogenesis of (1) two-compartment tumor metabolism and (2) mitochondrial biogenesis in human breast cancer cells.
机译：衰老会导致全身性氧化线粒体功能降低，从而使整个身体代谢向有氧糖酵解（也就是Warburg效应）转移。衰老也是包括乳腺癌在内的人类癌症发展的最重要风险因素之一。这两个发现如何关联？一个简单的想法是，癌细胞通过增加其氧化线粒体代谢（OXPHOS）的能力来抵抗衰老过程。然后，老化宿主中的局部和全身有氧糖酵解将提供能量丰富的线粒体燃料（例如L-乳酸和酮），以直接“促进”肿瘤细胞的生长和转移。这将建立一种与糖酵解/氧化代谢耦合的寄生虫-宿主关系或“两室肿瘤代谢”。癌细胞（“种子”）将在这种营养丰富的微环境（“土壤”）中蓬勃发展，该环境已通过宿主衰老而受精。在这种情况下，癌细胞仅试图通过线粒体代谢的放大来改造代谢变异，从而使自己免受衰老的影响。我们讨论Drs。的最新发现。 Ron DePinho（MD安德森）和Craig Thomspson（斯隆-​​凯特琳）也与这一新假说保持一致，将癌症的进展与代谢衰老联系在一起。使用数据挖掘和生物信息学方法，我们还提供了PGC1a / NRF1信号传导在人类乳腺癌细胞中（1）两室肿瘤代谢和（2）线粒体生物发生中的作用的关键证据。

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