Stretching Fibroblasts Remodels Fibronectin and Alters Cancer Cell Migration
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Most investigations of cancer-stroma interactions have focused on biochemical signaling effects, with much less attention being paid to biophysical factors. In this study, we investigated the role of mechanical stimuli on human prostatic fibroblasts using a microfluidic platform that was adapted for our experiments and further developed for both repeatable performance among multiple assays and for compatibility with high-resolution confocal microscopy. Results show that mechanical stretching of normal tissue-associated fibroblasts (NAFs) alters the structure of secreted fibronectin. Specifically, unstretched NAFs deposit and assemble fibronectin in a random, mesh-like arrangement, while stretched NAFs produce matrix with a more organized, linearly aligned structure. Moreover, the stretched NAFs exhibited an enhanced capability for directing co-cultured cancer cell migration in a persistent manner. Furthermore, we show that stretching NAFs triggers complex biochemical signaling events through the observation of increased expression of platelet derived growth factor receptor α (PDGFRα). A comparison of these behaviors with those of cancer-associated fibroblasts (CAFs) indicates that the observed phenotypes of stretched NAFs are similar to those associated with CAFs, suggesting that mechanical stress is a critical factor in NAF activation and CAF genesis.
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In vitro studies have shown that fibroblast stretching can activate SRF-driven transcription and YAP1-TEAD-driven transcription.
“In vitro studies have shown that fibroblast stretching, which may result from the hyperproliferation of transformed epithelial cells, can activate SRF-driven transcription and Yes-associated protein 1 (YAP1)–TEAD-driven transcription53,54,65,66.”
From A framework for advancing our understanding of cancer-associated fibroblasts (2020) · cites this paper as [65]
The Results and Discussion section reports that stretching human prostatic fibroblasts increased PDGFRα expression, supporting a biochemical response to stretching. It does not report activation of SRF-driven or YAP1–TEAD-driven transcription; searches for those factors and their full names found no such passage. No page numbers are available in our copy. (LLM, conf=0.84)
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- Authors
- Ao, M., Brewer, B. M., Yang, L., Franco Coronel, O. E., Hayward, S. W., Webb, D. J., & Li, D.
- Affiliations
- Vanderbilt University (US)
- Corresponding author
- Webb, Donna J.
- Li, Deyu
- Venue
- Scientific Reports
- Published
- 2015-02-09
- Volume
- 5
- Issue
- 1
- Pages
- 8334-8334
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC4321168
- OpenAlex
- W2053007259
- Cited by
- 96
- References
- 57
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 11 · 2023: 16 · 2022: 9 · 2021: 6 · 2020: 10 · 2019: 13 · 2018: 4 · 2017: 11 · 2016: 3 · 2015: 6
- FWCI
- 4.26
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Science Foundation (0909667)
- National Institutes of Health (1s10rr025524-01)
- National Cancer Institute (CA155572, R21CA155572)
- National Institute of General Medical Sciences (R01GM092914, GM092914)
- National Center for Research Resources (#S10RR025524)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- mechanical stretch, fibroblasts, tumor cell migration, tumor-stroma interactions, cancer-associated fibroblasts, PDGFRα signaling, microfluidic platform, prostate cancer, biophysical cues, extracellular matrix remodeling
- MeSH terms
- Cell Movement, Fibroblasts, Fibronectins, Humans, Male, Neoplasm Proteins, Prostatic Neoplasms, Tumor Cells, Cultured, Signal Transduction, Receptor, Platelet-Derived Growth Factor beta
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