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How cancer metabolism is tuned for proliferation and vulnerable to disruption

机译：如何调节癌症的新陈代谢以使其扩散并易于破坏

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By the mid-twentieth century, cancer cells were known to show characteristic alterations in their metabolic activity. These early studies resulted in the hypothesis that irreversible inac-tivation of respiration is causally involved in the development of tumours. Later, increased rates of glutaminolysis and lipid synthesis were found in tumour tissue, and the close association between cancer-cell metabolism and hypoxia was established (reviewed in ref. 2). Over the past decade, a more complex picture of cancer-cell metabolism has emerged. Many cancers show increased glucose uptake and enhanced glycolytic rates, suggesting that metabolic alteration provides a growth advantage for tumour cells. Some of these changes are similar to the metabolic response of non-transformed cells to growth-promoting signals, so it is not entirely clear whether these metabolic alterations are specific to cancer or just reflect the increased proliferation of tumour cells. However, different oncogenic signalling pathways target distinct components of the metabolic network. Moreover, tumours with the same genetic lesions have different metabolic profiles depending on the tissue they arise in, suggesting that the tissue environment strongly affects the metabolic activity of cancer cells. Altered metabolic activity is crucial for supporting uncontrolled proliferation, evasion of growth-inhibitory signals, cell migration and the dissemination of metastatic cells into distant tissues. However, metabolic reprogramming also renders cancer cells more susceptible to perturbations within the metabolic network. Identifying these metabolic dependencies could open a window of opportunity for therapeutic intervention.
机译：到20世纪中叶，已知癌细胞的代谢活性出现特征性变化。这些早期研究得出这样的假设，即不可逆地激活呼吸与肿瘤的发展有因果关系。后来，在肿瘤组织中发现了谷氨酰胺分解和脂质合成的速率增加，并且建立了癌细胞代谢与缺氧之间的密切联系（参见参考文献2）。在过去的十年中，出现了癌细胞代谢的更复杂的图景。许多癌症显示葡萄糖摄取增加和糖酵解速率增加，表明代谢改变为肿瘤细胞提供了生长优势。这些变化中的一些类似于未转化的细胞对促生长信号的代谢反应，因此，尚不清楚这些代谢变化是否是癌症特有的，还是仅反映了肿瘤细胞增殖的增加。但是，不同的致癌信号通路靶向代谢网络的不同组成部分。此外，具有相同遗传损伤的肿瘤具有不同的代谢特征，这取决于它们所处的组织，这表明组织环境强烈影响着癌细胞的代谢活性。代谢活性的改变对于支持不受控制的增殖，逃避生长抑制信号，细胞迁移以及转移性细胞向远处组织的扩散至关重要。但是，代谢重编程也使癌细胞更容易受到代谢网络内的干扰。识别这些代谢依赖性可以打开治疗干预的机会之窗。

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  • 来源
    《Nature》 |2012年第7424期|p.364-373|共10页
  • 作者

    Almut Schulze; Adrian L. Harris;

  • 作者单位

    Gene Expression Analysis Laboratory, Cancer Research UK, London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3LY, UK;

    Cancer Research UK Growth Factor Group, The Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Headington, Oxford OX3 9DS, UK;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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