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Related Experiment Video

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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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Tryptophan Modulation in Cancer-Associated Cachexia Mouse Models.

M Teresa Agulló-Ortuño1,2,3,4, Esther Mancebo5, Montserrat Grau6

  • 1Laboratory of Clinical and Translational Oncology, Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), Av. Córdoba s/n, 28041 Madrid, Spain.

International Journal of Molecular Sciences
|August 26, 2023
PubMed
Summary

Tryptophan metabolism is a promising target for managing cancer cachexia inflammation. Inhibiting tryptophan degradation improved systemic inflammation markers and immune cell activation in mouse models, though muscle wasting effects were not observed.

Keywords:
1-MTcachexiacancerinflammationmouse modelsskeletal muscletryptophan

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Area of Science:

  • Biochemistry
  • Oncology
  • Immunology

Background:

  • Cancer cachexia is a complex syndrome impacting patient survival and quality of life, with no effective treatments or clear pathophysiology.
  • Previous research indicated altered tryptophan metabolites in cachectic patients, suggesting a role for tryptophan in the syndrome.

Purpose of the Study:

  • To investigate the role of tryptophan metabolism in cancer-associated cachexia using syngeneic murine models (B16F10 melanoma and KPC pancreatic adenocarcinoma).
  • To evaluate the therapeutic potential of inhibiting tryptophan degradation in cancer cachexia.

Main Methods:

  • Established B16F10 and KPC murine models to induce cancer cachexia.
  • Assessed physiological and molecular markers of cachexia, including body weight, spleen weight, plasma proteins (MCP1, carbonylated proteins, CRP), myostatin, and skeletal muscle atrophy genes (Atrogin1).
  • Measured plasma tryptophan levels and analyzed immune cell populations (monocytes, lymphocytes, Tregs, CD8+ T cells) and their activation markers before and after treatment with 1-methyl-tryptophan (1-MT).

Main Results:

  • Murine models exhibited cachexia signs: reduced body weight, increased spleen weight, elevated MCP1 and carbonylated proteins. Skeletal muscle showed decreased weight and cross-sectional area, with increased atrophy gene expression.
  • Plasma tryptophan levels were significantly reduced in tumor-bearing mice and cachectic patients.
  • 1-MT treatment restored plasma tryptophan, improved splenomegaly and carbonylated protein levels, and modulated immune responses by reducing CCR2 expression on monocytes and activating lymphocytes, Tregs, and CD8+ T cells, indicating reduced systemic inflammation.
  • While 1-MT did not reverse muscle wasting, it preserved muscle functionality and promoted regeneration features.

Conclusions:

  • Tryptophan metabolism is dysregulated in cancer cachexia and contributes to systemic inflammation.
  • Inhibiting tryptophan degradation via 1-MT shows potential for modulating inflammation and improving immune status in cancer cachexia.
  • The tryptophan metabolic pathway represents a promising therapeutic target for managing inflammation associated with cancer cachexia.