ArticleClinical & experimental metastasis2017
Extracellular matrix 1 (ECM1) regulates the actin cytoskeletal architecture of aggressive breast cancer cells in part via S100A4 and Rho-family GTPases.
Article in Clinical & experimental metastasis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Biomarkers of tumor invasiveness in proteomics (Review).International journal of oncology · 2020Pooled it
- Article
- The Role of Actin-Binding Proteins in Breast Cancer Progression.Breast cancer (Dove Medical Press) · 2026Review
- Extracellular matrix protein 1 in cancer: multifaceted roles in tumor progression, prognosis, and therapeutic targeting.Archives of pharmacal research · 2025Review
- Extracellular Vesicle Proteome Analysis Improves Diagnosis of Recurrence in Triple-Negative Breast Cancer.Journal of extracellular vesicles · 2025Article
- Non-coding RNAs, a double-edged sword in breast cancer prognosis.Cancer cell international · 2025Review
- Enhancing Gene Delivery to Breast Cancer with Highly Efficient siRNA Loading and pH-Responsive Small Extracellular Vesicles.ACS biomaterials science & engineering · 2025Article
- NTRK fusion promotes tumor migration and invasion through epithelial-mesenchymal transition and closely interacts with ECM1 and NOVA1.BMC cancer · 2024Article
- Integrins as the pivotal regulators of cisplatin response in tumor cells.Cell communication and signaling : CCS · 2024Review
- Elevated extracellular matrix protein 1 in circulating extracellular vesicles supports breast cancer progression under obesity conditions.Nature communications · 2024Article
- Protein cargo in extracellular vesicles as the key mediator in the progression of cancer.Cell communication and signaling : CCS · 2024Review
- Article
- ECM1 and ANXA1 in urinary extracellular vesicles serve as biomarkers for breast cancer.Frontiers in oncology · 2024Article
- 3D bioprinted breast tumor-stroma models for pre-clinical drug testing.Materials today. Bio · 2023Article
- Extracellular Matrix Protein-1 as a Mediator of Inflammation-Induced Fibrosis After Myocardial Infarction.JACC. Basic to translational science · 2023Article
- Short communication: Photoperiod impacts ovarian extracellular matrix and metabolic gene expression in Siberian hamsters.Comparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2022Article
- Wentilactone A Reverses the NF-κB/ECM1 Signaling-Induced Cisplatin Resistance through Inhibition of IKK/IκB in Ovarian Cancer Cells.Nutrients · 2022Article
- Article
- Bioinformatics-based identification of miRNAs, mRNA, and regulatory signaling pathways involved in esophageal squamous cell carcinoma.Gastroenterology and hepatology from bed to bench · 2022Article
- Extracellular matrix protein-1 secretory isoform promotes ovarian cancer through increasing alternative mRNA splicing and stemness.Nature communications · 2021Observational
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
ECM1 overexpression is an independent predictor of poor prognosis in primary breast carcinomas, however the mechanisms by which ECM1 affects tumor progression have not been completely elucidated. ECM1 was silenced in the triple-negative breast cancer cell lines Hs578T and MDAMB231 using siRNA and the cells were evaluated for changes in morphology, migration, invasion and adhesion. Actin cytoskeleton alterations were evaluated by fluorescent staining and levels of activated Rho GTPases by pull down assays. ECM1 downregulation led to significantly diminished cell migration (p = 0.0005 for Hs578T and p = 0.02 for MDAMB231) and cell adhesion (p < 0.001 for Hs578T and p = 0.01 for MDAMB231). Cell invasion (matrigel) was reduced only in the Hs578T cells (p < 0.01). Silencing decreased the expression of the prometastatic molecules S100A4 and TGFβR2 in both cell lines and CD44 in Hs578T cells. ECM1-silenced cells also exhibited alterations in cell shape and showed bundles of F-actin across the cell (stress fibers) whereas NT-siRNA treated cells showed peripheral membrane ruffling. Downregulation of ECM1 was also associated with an increased F/G actin ratio, when compared to the cells transfected with NT siRNA (p < 0.001 for Hs578T and p < 0.00035 for MDAMB231) and a concomitant decline of activated Rho A in the Hs578T cells. Re-expression of S100A4 in ECM1-silenced cells rescued the phenotype in the Hs578T cells but not the MDAMB231 cells. We conclude that ECM1 is a key player in the metastatic process and regulates the actin cytoskeletal architecture of aggressive breast cancer cells at least in part via alterations in S100A4 and Rho A.
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