Cancer metabolism

Cancer metabolism refers to the alterations in cellular metabolism pathways that are evident in cancer cells compared with most normal tissue cells. Metabolic alterations in cancer cells are numerous and include aerobic glycolysis, reduced oxidative phosphorylation and the increased generation of biosynthetic intermediates needed for cell growth and proliferation.


Latest Research and Reviews

News and Comment

  • News and Views |

    Cancer cells require exogenous cysteine for proliferation and survival. In this issue of Nature Metabolism, Zhang et al. demonstrate that deletion of 5-methylthioadenosine phosphorylase promotes the synthesis of polyamines from methionine, thereby conferring sensitivity to cysteine starvation.

    • Joseph A. Combs
    •  & Gina M. DeNicola
  • News and Views |

    Caffa et al. report in Nature that hormone-receptor-positive breast cancer is sensitive to a form of ‘dietary augmentation therapy’ that implements periods of fasting, thus enhancing anti-cancer therapy.

    • Marcus D. Goncalves
    •  & Lewis C. Cantley
    Nature Metabolism 2, 559-560
  • Research Highlights |

    Using a rapid mass-spectrometry based approach to analyse aerosol released during surgical cauterization of tumour tissue, Koundouros et al. derived metabolic signatures associated with the tumour genotype. Based on these signatures, they identified a new mechanism by which oncogenic PI3K signalling promotes tumour growth.

    • Ulrike Harjes
  • News and Views |

    Pancreatic adenocarcinoma (PDAC) is often characterized by substantial amounts of fibrosis, and how these stromal components affect metabolite availability is not fully understood. Zhu et al. now show that cancer-associated fibroblasts consume branched-chain amino acids (BCAAs) at high levels but release corresponding branched-chain α-ketoacids that support PDAC cell growth.

    • Russell E. Ericksen
    •  & Weiping Han
  • News and Views |

    Selenium is a micronutrient essential for the generation of selenoproteins, which function predominantly by detoxifying cellular reactive oxygen species. In this issue, Carlisle et al. describe a novel mechanism whereby perturbing selenium utilization via inhibition of SEPHS2, a component of the selenocysteine-biosynthesis pathway, results in selenide poisoning and cancer cell death.

    • Anastasia Kapara
    • , Alessandro Vannini
    •  & Barrie Peck
    Nature Metabolism 2, 564-565