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Updated: Jun 14, 2026
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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
Proteome-Wide Dissection of Cachexia-Inducing Evolution in a Paired Human Neuroendocrine Carcinoma Cell Line Model
Julia Osaki1, Yomogi Shiota1, Kazuyoshi Yanagihara1
1Division of Rare Cancer Research, National Cancer Center, Tokyo, Japan.
Proteomics
|June 12, 2026
Summary
Cancer cachexia is an acquired tumor phenotype. Researchers identified specific tumor proteome changes linked to cachexia induction, offering new targets for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Proteomics
Background:
- Cancer cachexia is a severe systemic syndrome with poorly understood tumor-intrinsic drivers.
- Tumor evolution and its role in inducing cachexia require further investigation.
Purpose of the Study:
- To dissect the tumor evolution process that leads to cachexia induction.
- To identify specific proteomic changes within tumors associated with cachexia.
Main Methods:
- Utilized a paired model of human duodenal neuroendocrine carcinoma cell lines (TCC-NECT-2 and AkuNEC) with differing cachexia-inducing potential.
- Employed data-independent acquisition (DIA) proteomics to quantify and compare proteomes of cell lines and xenograft tumors.
- Performed lineage-specific and cross-lineage proteomic comparisons.
Main Results:
- Cachexia-inducing AkuNEC xenografts caused progressive body weight loss, unlike TCC-NECT-2 xenografts.
- Proteomic analysis revealed significant divergence between paired cell lines and extensive remodeling upon xenograft formation.
- Cachexia-inducing tumors showed in vivo enrichment for epithelial-mesenchymal transition, hypoxia, and cholesterol homeostasis pathways.
Conclusions:
- Cancer cachexia can be an acquired phenotype driven by in vivo tumor selection.
- The study provides a comprehensive proteome resource to identify tumor-intrinsic factors contributing to cachexia.
