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Published on: March 20, 2020
Relationship between galectin-3 expression and TRAIL sensitivity in breast cancer
Hope M Amm1, Donald J Buchsbaum
1Department of Radiation Oncology, University of Alabama at Birmingham, 1825 University Boulevard, Shelby, Room 701, Birmingham, AL 35294-2182, USA.
Expert Review of Anticancer Therapy
|September 16, 2011
Summary
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitivity in breast cancer depends on galectin-3 genotype. The His64 variant of galectin-3 enhances TRAIL-induced apoptosis, unlike the Pro64 variant.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in cancer cells via death receptors.
- Triple-negative breast cancer exhibits higher sensitivity to TRAIL-induced apoptosis compared to other subtypes.
- Galectin-3, associated with breast cancer incidence, has a polymorphism (His64/Pro64) whose role in TRAIL sensitivity is unexplored.
Discussion:
- This study investigates the impact of the galectin-3 His64/Pro64 polymorphism on breast cancer cell sensitivity to TRAIL.
- Breast cancer cell lines homozygous for Pro64 galectin-3 demonstrated resistance to TRAIL, while His64 homozygous lines showed sensitivity.
Key Insights:
- Galectin-3 genotype significantly influences TRAIL sensitivity in breast cancer.
- Transfection experiments confirmed that His64 galectin-3 confers TRAIL sensitivity, whereas Pro64 galectin-3 maintains resistance.
Outlook:
- Galectin-3 expression and genotype could serve as predictive biomarkers for TRAIL-based therapies and agonistic antibody treatments in breast cancer patients.
- Further research may explore targeted therapies based on galectin-3 status to improve patient outcomes.
