Prognostic and therapeutic implications of tumor-restrictive type III collagen in the breast cancer microenvironment
Collagen plays a critical role in regulating breast cancer progression and therapeutic resistance. An improved understanding of both the features and drivers of tumor-permissive and -restrictive collagen matrices are critical to improve prognostication and develop more effective therapeutic strategies. In this study, using a combination of in vitro, in vivo and bioinformatic experiments, we show that type III collagen (Col3) plays a tumor-restrictive role in human breast cancer. We demonstrate that Col3-deficient, human fibroblasts produce tumor-permissive collagen matrices that drive cell proliferation and suppress apoptosis in non-invasive and invasive breast cancer cell lines. In human triple-negative breast cancer biopsy samples, we demonstrate elevated deposition of Col3 relative to type I collagen (Col1) in non-invasive compared to invasive regions. Similarly, bioinformatics analysis of over 1000 breast cancer patient biopsies from The Cancer Genome Atlas BRCA cohort revealed that patients with higher Col3:Col1 bulk tumor expression had improved overall, disease-free, and progression-free survival relative to those with higher Col1:Col3 expression. Using an established 3D culture model, we show that Col3 increases spheroid formation and induces the formation of lumen-like structures that resemble non-neoplastic mammary acini. Finally, our in vivo study shows co-injection of murine breast cancer cells (4T1) with rhCol3-supplemented hydrogels limits tumor growth and decreases pulmonary metastatic burden compared to controls. Taken together, these data collectively support a tumor-suppressive role for Col3 in human breast cancer and suggest that strategies that increase Col3 may provide a safe and effective therapeutic modality to limit recurrence in breast cancer patients.
Authors
- Virginia F. Borges (ORCID: https://orcid.org/0000-0003-1158-7524)
- Ashton C. Berger
- Bassil Dekky (ORCID: https://orcid.org/0009-0008-8682-898X)
- Jason A. Burdick (ORCID: https://orcid.org/0000-0002-2006-332X)
- Daniel Stewart (ORCID: https://orcid.org/0000-0001-8248-4288)
- Massimo Cristofanilli (ORCID: https://orcid.org/0000-0002-4194-7175)
- Darko Stefanovski (ORCID: https://orcid.org/0000-0002-4654-0569)
- Edna Cukierman (ORCID: https://orcid.org/0000-0002-1452-9576)
- William Yen
- Becky K. Brisson (ORCID: https://orcid.org/0000-0002-5997-8412)
- Susan W. Volk (ORCID: https://orcid.org/0000-0003-3993-4145)
- Claudia Loebel (ORCID: https://orcid.org/0000-0002-3140-5663)
- Elizabeth A. Mauldin (ORCID: https://orcid.org/0000-0002-4718-6071)
- Charles‐Antoine Assenmacher (ORCID: https://orcid.org/0000-0003-0073-2730)
- C. QUINCEY
- Deborah Gillette
Institutions
- Fox Chase Cancer Center (US)
- University of Colorado Boulder (US)
- Cornell University (US)
- University of Michigan (US)
- University of Colorado Cancer Center (US)
- Weill Cornell Medicine (US)
- University of Colorado Anschutz Medical Campus (US)
- University of Pennsylvania (US)
- University of Colorado Denver (US)
Publication Details
- Journal
- npj Breast Cancer
- Published
- 2024-10-02
- DOI
- https://doi.org/10.1038/s41523-024-00690-y
- Citations
- 13
- Primary Topic
- Cell Adhesion Molecules Research
- Type
- article
- Field-Weighted Citation Impact
- 4.98
Funders
- University of Pennsylvania
- National Institutes of Health