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Tumors and Mitochondrial Respiration: A Neglected Connection

机译:肿瘤和线粒体呼吸:忽视连接

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For decades, tumor cells have been considered defective in mitochondrial respiration due to their dominant glycolytic metabolism. However, a growing body of evidence is now challenging this assumption, and also implying that tumors are metabolically less homogeneous than previously supposed. A small subpopulation of slow-cycling cells endowed with tumorigenic potential and multidrug resistance has been isolated from different tumors. Deep metabolic characterization of these tumorigenic cells revealed their dependency on mitochondrial respiration versus glycolysis, suggesting the existence of a common metabolic program active in slow-cycling cells across different tumors. These findings change our understanding of tumor metabolism and also highlight new vulnerabilities that can be exploited to eradicate cancer cells responsible for tumor relapse.
机译:几十年来,由于其优势糖酵解代谢,肿瘤细胞被认为是线粒体呼吸的缺陷。 然而,日益增长的证据现在挑战了这种假设,并且还暗示肿瘤的代谢性比以前所假设更不均匀。 从不同的肿瘤中分离出赋予致致瘤潜力和多药耐药性的慢循环细胞的小亚群。 这些致瘤细胞的深度代谢表征揭示了它们对线粒体呼吸与糖溶解的依赖性,这表明在不同肿瘤上的慢循环细胞中存在常见的代谢程序。 这些发现改变了我们对肿瘤新陈代谢的理解,并突出了可以利用负责肿瘤复发的癌细胞来利用的新脆弱性。

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