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Updated: Jan 22, 2026
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Orthotopic Implantation of Patient-Derived Cancer Cells in Mice Recapitulates Advanced Colorectal Cancer
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Smad3 mutant mice develop metastatic colorectal cancer
Y Zhu1, J A Richardson, L F Parada
1Center for Developmental Biology, UT Southwestern Medical Center, Dallas, Texas 75235-9133, USA.
Cell
|September 30, 1998
Summary
Transforming growth factor-beta (TGFbeta) signaling is crucial for cellular processes. Disruption of the Smad3 gene in mice leads to the development of aggressive colorectal cancer, offering a new model for human disease.
Area of Science:
- Molecular Biology
- Genetics
- Oncology
Background:
- Transforming growth factor-beta (TGFbeta) signaling pathways regulate critical cellular functions.
- Smad proteins (Smad2, Smad3, Smad4) are key mediators of TGFbeta signal transduction.
- Dysregulation of TGFbeta signaling is linked to various diseases, including cancer.
Purpose of the Study:
- To investigate the role of Smad3 in TGFbeta signaling.
- To generate and characterize Smad3-deficient mice.
- To determine the impact of Smad3 disruption on colorectal cancer development.
Main Methods:
- Cloning and targeted disruption of the mouse Smad3 gene.
- Generation of Smad3 mutant mice.
- Phenotypic analysis of Smad3 mutant mice, including tumor development and metastasis.
Main Results:
- Smad3 mutant mice are viable and fertile.
- Smad3 mutant mice develop spontaneous colorectal adenocarcinomas between 4 and 6 months of age.
- Tumors exhibit intestinal wall penetration and lymph node metastasis.
Conclusions:
- TGFbeta signaling, mediated by Smad3, plays a critical role in preventing colorectal cancer.
- Smad3 deficiency directly implicates TGFbeta signaling in colorectal cancer pathogenesis.
- Smad3 mutant mice provide a valuable animal model for studying human colorectal cancer.
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