Colorectal cancer (CRC) is one of the most common types of cancer worldwide. Despite recent advances in the molecular genetics of CRC, poor treatment outcomes highlight the need for a better understanding of the underlying mechanisms accounting for tumor initiation and progression. Recently, deregulation of cellular metabolism has emerged as a key hallmark of cancer. Reprogramming of core cellular metabolic pathways by cancer cells provides energy, anaplerotic precursors and reducing equivalents required to support tumor growth. Here, we review key findings implicating cancer metabolism as a major contributor of tumor initiation, growth and metastatic dissemination in CRC. We summarize the metabolic pathways governing stem cell fate in the intestine, the metabolic adaptations of proliferating colon cancer cells and their crosstalk with oncogenic signaling, and how they fulfill the energetic demands imposed by the metastatic cascade. Lastly, we discuss how some of these metabolic pathways could represent new vulnerabilities of CRC cells with the potential to be targeted.

中文翻译：

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调节大肠癌发生和发展的代谢途径。

大肠癌（CRC）是全球最常见的癌症类型之一。尽管CRC的分子遗传学最近取得了进展，但不良的治疗结果凸显了需要更好地了解导致肿瘤发生和发展的潜在机制的必要性。最近，细胞代谢失调已成为癌症的关键标志。癌细胞对核心细胞代谢途径的重编程可提供能量，抗动脉粥样硬化前体并减少支持肿瘤生长所需的等效物质。在这里，我们审查了关键的发现，暗示癌症的代谢是CRC中肿瘤起始，生长和转移性扩散的主要因素。我们总结了控制肠道干细胞命运的代谢途径，增殖结肠癌细胞的代谢适应以及它们与致癌信号的串扰，以及它们如何满足转移级联所施加的能量需求。最后，我们讨论了这些代谢途径中的某些途径如何能代表具有潜在针对性的CRC细胞新弱点。