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

  • Research | | open

    Cancer subtypes may have distinct metabolic vulnerabilities that can be exploited for therapeutic interventions. Here, the authors show that in lung cancer, genetic activation of distinct oncogenic receptor tyrosine kinases results in unique metabolic liabilities and, in particular, EGFR aberrant cancers rely on the serine biosynthetic pathway while FGFR aberrant cancers rely on glycolysis.

    • Nan Jin
    • , Aiwei Bi
    • , Xiaojing Lan
    • , Jun Xu
    • , Xiaomin Wang
    • , Yingluo Liu
    • , Ting Wang
    • , Shuai Tang
    • , Hanlin Zeng
    • , Ziqi Chen
    • , Minjia Tan
    • , Jing Ai
    • , Hua Xie
    • , Tao Zhang
    • , Dandan Liu
    • , Ruimin Huang
    • , Yue Song
    • , Elaine Lai-Han Leung
    • , Xiaojun Yao
    • , Jian Ding
    • , Meiyu Geng
    • , Shu-Hai Lin
    •  & Min Huang
  • Research | | open

    Cancer cells must develop distinct metabolic adaptations to survive in challenging metastatic environments. Here, the authors find, via an in vivo RNAi screen, that the aldo-keto reductase AKR1B10 limits the toxic side effects of oxidative stress to sustain fatty acid oxidation and promote metastatic colonisation.

    • Antoinette van Weverwijk
    • , Nikolaos Koundouros
    • , Marjan Iravani
    • , Matthew Ashenden
    • , Qiong Gao
    • , George Poulogiannis
    • , Ute Jungwirth
    •  & Clare M. Isacke
  • Research | | open

    Metabolic rewiring is a feature of many cancers. Here, the authors combine control theory and flux correlation analysis to study the transition of healthy metabolic networks to cancer states, and find that cancer metabolism is characterized by more streamlined flux distributions.

    • Jean-Marc Schwartz
    • , Hiroaki Otokuni
    • , Tatsuya Akutsu
    •  & Jose C. Nacher
  • Research | | open

    Tobias Ackermann et al. show that the C/EBPβ Liver-enriched inhibitory protein (LIP) induces aerobic glycolysis and mitochondrial respiration by suppressing the let-7 microRNA family that targets the Lin28b-mRNA. This study identifies LIP as a regulator of metabolic reprogramming that is reminiscent of cancer metabolism.

    • Tobias Ackermann
    • , Götz Hartleben
    • , Christine Müller
    • , Guido Mastrobuoni
    • , Marco Groth
    • , Britt A. Sterken
    • , Mohamad A. Zaini
    • , Sameh A. Youssef
    • , Hidde R. Zuidhof
    • , Sara R. Krauss
    • , Gertrud Kortman
    • , Gerald de Haan
    • , Alain de Bruin
    • , Zhao-Qi Wang
    • , Matthias Platzer
    • , Stefan Kempa
    •  & Cornelis F. Calkhoven
  • Research | | open

    Cancer cells develop specific metabolic adaptations. Here, the authors show that in prostate cancer models, the ubiquitin ligase Hect9 promotes tumor growth by accelerating glucose metabolism via ubiquitination of Hexokinase 2, a central regulator of glycolysis.

    • Hong-Jen Lee
    • , Chien-Feng Li
    • , Diane Ruan
    • , Jiabei He
    • , Emily D. Montal
    • , Sonja Lorenz
    • , Geoffrey D. Girnun
    •  & Chia-Hsin Chan
  • Research | | open

    The ribosomal protein RPL10 is frequently mutated in T-cell acute lymphoblastic leukemia (T-ALL). Here, the authors show that it promotes proliferation of T-ALL cells by upregulating the serine biosynthesis enzyme phosphoserine phosphatase which in turn modulates serine and glycine metabolism.

    • Kim R. Kampen
    • , Laura Fancello
    • , Tiziana Girardi
    • , Gianmarco Rinaldi
    • , Mélanie Planque
    • , Sergey O. Sulima
    • , Fabricio Loayza-Puch
    • , Benno Verbelen
    • , Stijn Vereecke
    • , Jelle Verbeeck
    • , Joyce Op de Beeck
    • , Jonathan Royaert
    • , Pieter Vermeersch
    • , David Cassiman
    • , Jan Cools
    • , Reuven Agami
    • , Mark Fiers
    • , Sarah-Maria Fendt
    •  & Kim De Keersmaecker

News and Comment

  • Research Highlights |

    In a study published in Science Translational Medicine, Zhang et al. report a mechanism of ibrutinib resistance in mantle cell lymphoma that involves metabolic reprogramming towards glutamine-fuelled oxidative phosphorylation, revealing a novel therapeutic opportunity.

    • Conor A. Bradley
  • News |

    Bioluminescence lights her way to measure glucose uptake in vivo, and why a chemist travels outside her comfort zone.

    • Vivien Marx
    Nature Methods 16, 449
  • Research Highlights |

    Two studies show that in the presence of KRAS pathway inhibition, KRAS-mutant pancreatic ductal adenocarcinomas become dependent on autophagy for survival. Removing this protective mechanism through combining MEK or ERK inhibitors with inhibitors of autophagy is likely to be therapeutically beneficial.

    • Sarah Seton-Rogers