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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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Published on: November 30, 2016

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Targeting of Fn14 Prevents Cancer-Induced Cachexia and Prolongs Survival

Amelia J Johnston1, Kate T Murphy2, Laura Jenkinson1

  • 1Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC 3086, Australia.

Cell
|September 12, 2015
PubMed

Insights

Targeting the tumor necrosis factor (TNF) superfamily member Fn14 with antibodies can combat cancer cachexia. This approach inhibits weight loss and improves lifespan by preventing inflammation and muscle wasting in cancer patients.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Tumor necrosis factor-weak (TWEAK) and its receptor Fn14 are upregulated in tumors.
  • Fn14 expression in tumors is linked to cachexia, a wasting syndrome.

Purpose of the Study:

  • To investigate the role of Fn14 signaling in tumor-induced cachexia.
  • To evaluate the therapeutic potential of anti-Fn14 antibodies in treating cancer cachexia.

Main Methods:

  • Utilized mouse models with tumors expressing Fn14.
  • Administered antibodies targeting Fn14.
  • Assessed tumor growth, weight loss, inflammation, and muscle/fat mass.
  • Compared cachexia development in wild-type versus Fn14- and TWEAK-deficient hosts.

Main Results:

  • Anti-Fn14 antibodies significantly extended lifespan by inhibiting tumor-induced weight loss.
  • Antibodies reduced tumor-induced inflammation and loss of fat and muscle mass.
  • Fn14 signaling within the tumor, not the host, drives cachexia.

Conclusions:

  • Fn14 plays a critical role in the etiology of cancer cachexia.
  • Anti-Fn14 antibodies represent a promising therapeutic strategy for cachexia.
  • Targeting Fn14 may improve quality of life and survival for cancer patients.

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