ArticleThe Journal of cell biology2005
Growth factor-induced shedding of syndecan-1 confers glypican-1 dependence on mitogenic responses of cancer cells.
Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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.
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Who cites it
70 citing papers in PubMed, 121 citations in OpenAlex.
- Serum matrix metalloproteinase-7, Syndecan-1, and CA 19-9 as a biomarker panel for diagnosis of pancreatic ductal adenocarcinoma.Cancer medicine · 2024Article
- Unraveling the Mechanisms Involved in the Beneficial Effects of Magnesium Treatment on Skin Wound Healing.International journal of molecular sciences · 2024Article
- Dichotomous Effects of Glypican-4 on Cancer Progression and Its Crosstalk with Oncogenes.International journal of molecular sciences · 2024Article
- Heparan sulfate proteoglycans in cancer: Pathogenesis and therapeutic potential.Advances in cancer research · 2023Article
- Targeting syndecan-1: new opportunities in cancer therapy.American journal of physiology. Cell physiology · 2022Review
- Prognostic impact of the glypican family of heparan sulfate proteoglycans on the survival of breast cancer patients.Journal of cancer research and clinical oncology · 2021Article
- Diagnostic, Predictive and Prognostic Molecular Biomarkers in Pancreatic Cancer: An Overview for Clinicians.Cancers · 2021Review
- Syndecans and Pancreatic Ductal Adenocarcinoma.Biomolecules · 2021Review
- High glypican-1 expression is a prognostic factor for predicting a poor clinical prognosis in patients with hepatocellular carcinoma.Oncology letters · 2020Article
- Syndecan-1 Promotes Hepatocyte-Like Differentiation of Hepatoma Cells Targeting Ets-1 and AP-1.Biomolecules · 2020Article
- Heparan Sulfate Proteoglycans: Key Mediators of Stem Cell Function.Frontiers in cell and developmental biology · 2020Review
- Proteoglycans Are Attractive Biomarkers and Therapeutic Targets in Hepatocellular Carcinoma.International journal of molecular sciences · 2018Review
- TRPM2 promotes the proliferation and invasion of pancreatic ductal adenocarcinoma.Molecular medicine reports · 2018Article
- Dually modified transmembrane proteoglycans in development and disease.Cytokine & growth factor reviews · 2018Review
- The clinical significance of circulating GPC1 positive exosomes and its regulative miRNAs in colon cancer patients.Oncotarget · 2017Article
- The role of heparins and nano-heparins as therapeutic tool in breast cancer.Glycoconjugate journal · 2017Review
- Elevated glypican-1 expression is associated with an unfavorable prognosis in pancreatic ductal adenocarcinoma.Cancer medicine · 2017Article
- α3 Chains of type V collagen regulate breast tumour growth via glypican-1.Nature communications · 2017Article
- Inflammation and Epithelial-Mesenchymal Transition in Pancreatic Ductal Adenocarcinoma: Fighting Against Multiple Opponents.Cancer growth and metastasis · 2017Review
- Mechanisms of heparanase inhibitors in cancer therapy.Experimental hematology · 2016Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The cell surface heparan sulfate proteoglycan (HSPG) glypican-1 is up-regulated by pancreatic and breast cancer cells, and its removal renders such cells insensitive to many growth factors. We sought to explain why the cell surface HSPG syndecan-1, which is also up-regulated by these cells and is a known growth factor coreceptor, does not compensate for glypican-1 loss. We show that the initial responses of these cells to the growth factor FGF2 are not glypican dependent, but they become so over time as FGF2 induces shedding of syndecan-1. Manipulations that retain syndecan-1 on the cell surface make long-term FGF2 responses glypican independent, whereas those that trigger syndecan-1 shedding make initial FGF2 responses glypican dependent. We further show that syndecan-1 shedding is mediated by matrix metalloproteinase-7 (MMP7), which, being anchored to cells by HSPGs, also causes its own release in a complex with syndecan-1 ectodomains. These results support a specific role for shed syndecan-1 or MMP7-syndecan-1 complexes in tumor progression and add to accumulating evidence that syndecans and glypicans have nonequivalent functions in vivo.
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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.