ArticleMatrix biology : journal of the International Society for Matrix Biology2017
Breast cancer cells alter the dynamics of stromal fibronectin-collagen interactions.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 104 citations in OpenAlex.
- Obesity, Inflammation, and Tumor Microenvironment in Three-Dimensional Models of Breast Cancer.Cells · 2026Review
- Molecular biology of targeting lymphangiogenesis in cancer: Therapeutic strategies and future promise.Fundamental research · 2026Review
- Hybrid Scaffolds Decouple Biochemical & Biophysical Regulation of Cell Phenotype.Advanced healthcare materials · 2026Article
- Remodeling the tumor dormancy ecosystem to prevent recurrence and metastasis.Signal transduction and targeted therapy · 2026Review
- Orchestrating the pre-metastatic niche: roles of stromal mediators and immune cells in metastatic progression and therapeutic targeting.Frontiers in immunology · 2026Review
- Minimal Residual Disease in Breast Cancer: Tumour Microenvironment Interactions, Detection Methods and Therapeutic Approaches.International journal of molecular sciences · 2025Review
- Tumor-Associated Macrophages and Collagen Remodeling in Mammary Carcinomas: A Comparative Analysis in Dogs and Humans.International journal of molecular sciences · 2025Article
- Inhibiting fibronectin assembly in the breast tumor microenvironment increases cell death and improves response to doxorubicin.bioRxiv : the preprint server for biology · 2025Article
- Comparative evaluation of collagen modifications in breast cancer in human and canine carcinomas.Scientific reports · 2024Article
- Cancer-associated fibroblasts (CAFs) gene signatures predict outcomes in breast and prostate tumor patients.Journal of translational medicine · 2024Article
- IFIT1 + neutrophil is a causative factor of immunosuppressive features of poorly cohesive carcinoma (PCC).Journal of translational medicine · 2024Article
- Simultaneous fingerprinting of multiplex collagen biomarkers in connective tissues by multicolor quantum dots-based peptide probes.Materials today. Bio · 2024Article
- Engineering approaches for understanding mechanical memory in cancer metastasis.APL bioengineering · 2024Review
- Multiple aspects of matrix stiffness in cancer progression.Frontiers in oncology · 2024Review
- Collagen modifications predictive of lymph node metastasis in dogs with carcinoma in mixed tumours.Frontiers in veterinary science · 2024Article
- Reprogramming of VEGF-mediated extracellular matrix changes through autocrine signaling.Cancer biology & therapy · 2023Article
- Matrix Stiffness Regulated Endoplasmic Reticulum Stress-mediated Apoptosis of Osteosarcoma Cell through Ras Signal Cascades.Cell biochemistry and biophysics · 2023Article
- Implications of Cellular Mechanical Memory in Bioengineering.ACS biomaterials science & engineering · 2023Review
- Wnt signaling: a double-edged sword in protecting bone from cancer.Journal of bone and mineral metabolism · 2023Review
- Updates on Lymphovascular Invasion in Breast Cancer.Biomedicines · 2023Review
6 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Breast cancer cells recruit surrounding stromal cells, such as cancer-associated fibroblasts (CAFs), to remodel their extracellular matrix (ECM) and promote invasive tumor growth. Two major ECM components, fibronectin (Fn) and collagen I (Col I), are known to interact with each other to regulate cellular behavior. In this study, we seek to understand how Fn and Col I interplay and promote a dysregulated signaling pathway to facilitate tumor progression. Specifically, we investigated the evolution of tumor-conditioned stromal ECM composition, structure, and relaxation. Furthermore, we assessed how evolving Fn-Col I interactions gradually affected pro-angiogenic signaling. Our data first indicate that CAFs initially assembled a strained, viscous, and unfolded Fn matrix. This early altered Fn matrix was later remodeled into a thick Col I-rich matrix that was characteristic of a dense tumor mass. Next, our results suggest that this ECM remodeling was primarily mediated by matrix metalloproteinases (MMPs). This MMP activity caused profound structural and mechanical changes in the developing ECM, which then modified vascular endothelial growth factor (VEGF) secretion by CAFs and matrix sequestration. Collectively, these findings enhance our understanding of the mechanisms by which Fn and Col I synergistically interplay in promoting a sustained altered signaling cascade to remodel the breast tumor stroma for invasive breast tumor growth.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.