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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Published on: November 30, 2016

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Decreased liver B vitamin-related enzymes as a metabolic hallmark of cancer cachexia

Yasushi Kojima1, Emi Mishiro-Sato2, Teruaki Fujishita2

  • 1Division of Pathophysiology, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya, Aichi, 464-8681, Japan. ykojima@aichi-cc.jp.

Nature Communications
|October 6, 2023
PubMed

Insights

Cancer cachexia involves metabolic changes, including reduced B vitamin liver enzymes and metabolites like niacin and vitamin B6. These findings in mice and cancer patients highlight key metabolic alterations in cachexia.

Area of Science:

  • Biochemistry
  • Oncology
  • Metabolomics

Background:

  • Cancer cachexia is a severe metabolic disorder causing approximately 20% of cancer-related deaths.
  • The metabolic alterations underlying cancer cachexia remain largely uncharacterized.

Purpose of the Study:

  • To investigate the unexplored metabolic landscape of cancer cachexia.
  • To identify key metabolic changes and their molecular basis in cachexia.

Main Methods:

  • Utilized metabolomics and proteomics in multiple mouse models of cancer cachexia.
  • Analyzed liver and blood samples for metabolite and enzyme profiling.
  • Performed protein post-translational modification analysis to identify changes like malonylation.

Main Results:

  • Identified decreased levels of niacin, vitamin B6, and glycine-related one-carbon metabolites in the liver.
  • Demonstrated a linear correlation between reduced B vitamin-dependent liver enzymes and their corresponding metabolites.
  • Observed decreased protein malonylation and confirmed these metabolic/proteomic changes in blood from mouse models and gastric cancer patients with cachexia.

Conclusions:

  • Reduced B vitamin-related liver enzymes and metabolites are a hallmark of cancer cachexia.
  • These changes are linked to protein abundance, cofactor availability, and decreased protein malonylation.
  • Findings highlight the clinical relevance of these metabolic alterations in cancer cachexia.

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