ArticleCancer research2008
Membrane type 1 matrix metalloproteinase-mediated stromal syndecan-1 shedding stimulates breast carcinoma cell proliferation.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
- Spatial proteo-transcriptomic profiling reveals the molecular landscape of borderline ovarian tumors and their invasive progression.Cancer cell · 2025Article
- Shed Syndecan-4 and Its Possible Roles in Osteoarthritis.Biomedicines · 2025Review
- Redefining metalloproteases specificity through network proteolysis.Trends in molecular medicine · 2024Review
- Revisiting the Syndecans: Master Signaling Regulators with Prognostic and Targetable Therapeutic Values in Breast Carcinoma.Cancers · 2023Review
- Targeting syndecan-1: new opportunities in cancer therapy.American journal of physiology. Cell physiology · 2022Review
- The Glycobiology of Pulmonary Arterial Hypertension.Metabolites · 2022Review
- Cleavage of Syndecan-1 Promotes the Proliferation of the Basal-Like Breast Cancer Cell Line BT-549 Via Akt SUMOylation.Frontiers in cell and developmental biology · 2021Article
- Emerging Role of Syndecans in Extracellular Matrix Remodeling in Cancer.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Heparan Sulfate Proteoglycans Biosynthesis and Post Synthesis Mechanisms Combine Few Enzymes and Few Core Proteins to Generate Extensive Structural and Functional Diversity.Molecules (Basel, Switzerland) · 2020Review
- SDC1 promotes cisplatin resistance in hepatic carcinoma cells via PI3K-AKT pathway.Human cell · 2020Article
- Syndecan-1 induction in lung microenvironment supports the establishment of breast tumor metastases.Breast cancer research : BCR · 2018Article
- Comparison of Syndecan-1 Immunohistochemical Expression in Lobular and Ductal Breast Carcinoma with Nodal Metastases.Analytical cellular pathology (Amsterdam) · 2018Article
- Biomarkers of Glycocalyx Injury are Associated with Delayed Cerebral Ischemia Following Aneurysmal Subarachnoid Hemorrhage: A Case Series Supporting a New Hypothesis.Neurocritical care · 2017Article
- Proteoglycans: Potential Agents in Mammographic Density and the Associated Breast Cancer Risk.Journal of mammary gland biology and neoplasia · 2015Review
- Elucidation of the CHO Super-Ome (CHO-SO) by Proteoinformatics.Journal of proteome research · 2015Article
- Molecular and clinical profiles of syndecan-1 in solid and hematological cancer for prognosis and precision medicine.Oncotarget · 2015Review
- Insights into the key roles of proteoglycans in breast cancer biology and translational medicine.Biochimica et biophysica acta · 2015Review
- Membrane-Type 1 Matrix Metalloproteinase Downregulates Fibroblast Growth Factor-2 Binding to the Cell Surface and Intracellular Signaling.Journal of cellular physiology · 2015Article
- Shed Syndecan-1 is involved in chemotherapy resistance via the EGFR pathway in colorectal cancer.British journal of cancer · 2014Article
- Diagnostic and prognostic value of soluble syndecan-1 in pleural malignancies.BioMed research international · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mounting evidence implicates stromal fibroblasts in breast carcinoma progression. We have recently shown in three-dimensional coculture experiments that human mammary fibroblasts stimulate the proliferation of T47D breast carcinoma cells and that this activity requires the shedding of the heparan sulfate proteoglycan syndecan-1 (Sdc1) from the fibroblast surface. The goal of this project was to determine the mechanism of Sdc1 ectodomain shedding. The broad spectrum matrix metalloproteinase (MMP) inhibitor GM6001 specifically blocked Sdc1-mediated carcinoma cell growth stimulation, pointing toward MMPs as critical enzymes involved in Sdc1 shedding. MMP-2 and membrane type 1 MMP (MT1-MMP) were the predominant MMPs expressed by the mammary fibroblasts. Fibroblast-dependent carcinoma cell growth stimulation in three-dimensional coculture was abolished by MT1-MMP expression silencing with small interfering RNA and restored either by adding recombinant MT1-MMP catalytic domain or by expressing a secreted form of Sdc1 in the fibroblasts. These findings are consistent with a model where fibroblast-derived MT1-MMP cleaves Sdc1 at the fibroblast surface, leading to paracrine growth stimulation of carcinoma cells by Sdc1 ectodomain. The relevance of MT1-MMP in paracrine interactions was further supported by coculture experiments with T47D cells and primary fibroblasts isolated from human breast carcinomas or matched normal breast tissue. Carcinoma-associated fibroblasts stimulated T47D cell proliferation significantly more than normal fibroblasts in three-dimensional coculture. Function-blocking anti-MT1-MMP antibody significantly inhibited the T47D cell growth stimulation in coculture with primary fibroblasts. In summary, these results ascribe a novel role to fibroblast-derived MT1-MMP in stromal-epithelial signaling in breast carcinomas.
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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.