ArticleInternational journal of molecular sciences2020
Extracellular Matrix Derived from High Metastatic Human Breast Cancer Triggers Epithelial-Mesenchymal Transition in Epithelial Breast Cancer Cells through αvβ3 Integrin.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
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- Transforming growth factor-β and integrins: key players in EMT and breast cancer progression.Cancer cell international · 2026Review
- Diagnostic and prognostic values of differentially expressed genes in canine mammary carcinoma: An integrated bioinformatics analysis.PloS one · 2026Article
- Calumenin, A Calcium-Binding Modulatory Protein, Effective in Pathological Calcifications and Cancers, With Therapeutic Application Promise.FASEB bioAdvances · 2025Review
- miR-3606-3p alleviates skin fibrosis by integratively suppressing the integrin/FAK, p-AKT/p-ERK, and TGF-β signaling cascades.Journal of advanced research · 2025Article
- Silencing Calumenin Expression via Artificial MicroRNA, a Potential Breakthrough for Inhibiting Proliferation, Halting Migration, and Triggering Apoptosis in Breast Cancer Cells.Advanced pharmaceutical bulletin · 2025Article
- Disulfide bond-related gene signature development for bladder cancer prognosis prediction and immune microenvironment characterization.Scientific reports · 2025Article
- Effects of Acidic Polysaccharide-Enriched Extracts fromBiology · 2025Article
- Circular RNA circHSPA8 Aggravates Metastasis by Acting as a Competitive Inhibitor of miR-195-5p to Upregulate WNT3A Expression in Breast Cancer.Journal of cellular and molecular medicine · 2025Article
- Missense mutations of GPER1 in breast invasive carcinoma: Exploring gene expression, signal transduction and immune cell infiltration with insights from cellular pharmacology.Biomedical reports · 2025Article
- Transcriptomics and proteomics association analysis demystify the molecular mechanisms underlying epididymal sperm maturation disorders in yaks with cryptorchidism.Journal of animal science · 2025Article
- A switch from α5β1 to αvβ3 integrin activity contributes to the development of a profibrotic mesenchymal phenotype in trabecular meshwork cells.Frontiers in cell and developmental biology · 2025Article
- Targeting E3 ubiquitin ligases: a new frontier in idiopathic pulmonary fibrosis treatment.Frontiers in immunology · 2025Review
- HMCN1 as a conserved biomarker of epithelial-mesenchymal transition: a cross-cancer analysis.Frontiers in oncology · 2025Article
- Development of a 3D tumor model based on decellularized matrix using high-throughput approaches.Frontiers in bioengineering and biotechnology · 2025Review
- Multimodal mechano-microscopy reveals mechanical phenotypes of breast cancer spheroids in three dimensions.APL bioengineering · 2024Article
- Extracellular matrix remodeling in tumor progression and immune escape: from mechanisms to treatments.Molecular cancer · 2023Review
- Article
- Serum mitochondrial tsRNA serves as a novel biomarker for hepatocarcinoma diagnosis.Frontiers of medicine · 2022Article
- A gene expression signature in HER2+ breast cancer patients related to neoadjuvant chemotherapy resistance, overall survival, and disease-free survival.Frontiers in genetics · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Alterations in the composition and architecture of the extracellular matrix (ECM) can influence cancer growth and dissemination. During epithelial-mesenchymal transition (EMT), epithelial cells assume a mesenchymal cell phenotype, changing their adhesion profiles from cell-cell contacts to cell-matrix interactions, contributing to metastasis. Breast cancer cells present at different stages of differentiation, producing distinct ECMs in the same tumor mass. However, the contribution of ECM derived from metastatic tumor cells to EMT is unclear. Here, we showed the mechanisms involved in the interaction of MCF-7, a low-metastatic, epithelial breast cancer cell line, with the ECM produced by a high metastatic breast tumor cell, MDA-MB-231 (MDA-ECM). MDA-ECM induced morphological changes in MCF-7 cells, decreased the levels of E-cadherin, up-regulated mesenchymal markers, and augmented cell migration. These changes were accompanied by the activation of integrin-associated signaling, with increased phosphorylation of FAK, ERK, and AKT and activation canonical TGF-β receptor signaling, enhancing phosphorylation of SMAD2 and SMAD4 nuclear translocation in MCF-7 cells. Treatment with Kistrin (Kr), a specific ligand of integrin αvβ3 EMT induced by MDA-ECM, inhibited TGF-β receptor signaling in treated MCF-7 cells. Our results revealed that after interaction with the ECM produced by a high metastatic breast cancer cell, MCF-7 cells lost their characteristic epithelial phenotype undergoing EMT, an effect modulated by integrin signaling in crosstalk with TGF-β receptor signaling pathway. The data evidenced novel potential targets for antimetastatic breast cancer therapies.
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