ArticleMolecular cancer research : MCR2014
TIMP-1 via TWIST1 induces EMT phenotypes in human breast epithelial cells.
Article in Molecular cancer research : MCR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 77 citations in OpenAlex.
- Machine Learning-Based Identification of Survival-Associated CpG Biomarkers in Pancreatic Ductal Adenocarcinoma.Journal of precision medicine (Amsterdam, Netherlands) · 2026Article
- Twist1 overexpression models an aggressive subtype of pancreatic ductal adenocarcinoma in vivo.Lab animal · 2026Article
- Bioinformatic Analysis of Contrasting Expression Patterns and Molecular Interactions of TIMPs in Breast Cancer: Implications for Tumor Progression and Survival.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Integrin-Mediated TIMP1 Signaling Reprograms Liver Macrophages and Accelerates Colorectal Cancer Metastasis.Cells · 2025Article
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- Human hypofunctional NCF1 variants promote pulmonary fibrosis in the bleomycin-induced mouse model and patients with systemic sclerosis via expansion of SPP1Annals of the rheumatic diseases · 2025Article
- Tissue inhibitor of metalloproteinase 1 as a biomarker of venous invasion in pancreatic ductal adenocarcinoma.American journal of cancer research · 2025Article
- Benzophenone-3 alters expression of genes encoding vascularization and epithelial-mesenchymal transition functions during Trp53-null mammary tumorigenesis.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2024Article
- Glutamate is effective in decreasing opacity formed in galactose-induced cataract model.Scientific reports · 2024Article
- Clinicopathological features associated with CD44 and CD63 expression in breast cancer.Ecancermedicalscience · 2024Article
- Irisin: A Possible Marker of Adipose Tissue Dysfunction in Obesity.International journal of molecular sciences · 2023Article
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- A straightforward method to quantify circulating mRNAs as biomarkers of colorectal cancer.Scientific reports · 2023Article
- FAM83B promotes the invasion of primary lung adenocarcinoma via PI3K/AKT/NF-κB pathway.BMC pulmonary medicine · 2023Article
- Proteins Found in the Triple-Negative Breast Cancer Secretome and Their Therapeutic Potential.International journal of molecular sciences · 2023Review
- Cardiac Glycoside Oleandrin Suppresses EMT Ability in Endometrial Carcinoma Cells.International journal of molecular and cellular medicine · 2023Article
- Osteoblast Secretome Modulated by Abiraterone Treatment Affects Castration Resistant Prostate Cancer Cell Proliferation.Biomedicines · 2022Article
- The Repertoire of Tissue Inhibitors of Metalloproteases: Evolution, Regulation of Extracellular Matrix Proteolysis, Engineering and Therapeutic Challenges.Life (Basel, Switzerland) · 2022Review
- Cooperative interaction between ERα and the EMT-inducer ZEB1 reprograms breast cancer cells for bone metastasis.Nature communications · 2022Article
- Matrix metalloproteinases as therapeutic targets in breast cancer.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledTissue inhibitor of metalloproteinase-1 (TIMP-1) regulates intracellular signaling networks for inhibition of apoptosis. Tetraspanin (CD63), a cell surface binding partner for TIMP-1, was previously shown to regulate integrin-mediated survival pathways in the human breast epithelial cell line MCF10A. In the current study, we show that TIMP-1 expression induces phenotypic changes in cell morphology, cell adhesion, cytoskeletal remodeling, and motility, indicative of an epithelial-mesenchymal transition (EMT). This is evidenced by loss of the epithelial cell adhesion molecule E-cadherin with an increase in the mesenchymal markers vimentin, N-cadherin, and fibronectin. Signaling through TIMP-1, but not TIMP-2, induces the expression of TWIST1, an important EMT transcription factor known to suppress E-cadherin transcription, in a CD63-dependent manner. RNAi-mediated knockdown of TWIST1 rescued E-cadherin expression in TIMP-1-overexpressing cells, demonstrating a functional significance of TWIST1 in TIMP-1-mediated EMT. Furthermore, analysis of TIMP-1 structural mutants reveals that TIMP-1 interactions with CD63 that activate cell survival signaling and EMT do not require the matrix metalloproteinase (MMP)-inhibitory domain of TIMP-1. Taken together, these data demonstrate that TIMP-1 binding to CD63 activates intracellular signal transduction pathways, resulting in EMT-like changes in breast epithelial cells, independent of its MMP-inhibitory function. IMPLICATIONS: TIMP-1's function as an endogenous inhibitor of MMP or as a "cytokine-like" signaling molecule may be a critical determinant for tumor cell behavior.
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