ArticleMatrix biology : journal of the International Society for Matrix Biology2014
Chemotherapy stimulates syndecan-1 shedding: a potentially negative effect of treatment that may promote tumor relapse.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 67 citations in OpenAlex.
- Methamphetamine-Induced Loss of Syndecan-1 and Retinal Endothelial Integrity via the TAAR-1/MMP-9 Pathway.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Article
- Current Anti-Myeloma Chimeric Antigen Receptor-T Cells: Novel Targets and Methods.Balkan medical journal · 2025Review
- SDC1 is a critical transmembrane proteoglycan in breast cancer.World journal of surgical oncology · 2025Review
- Profilin 1 induces drug resistance by downregulating CD138 expression via autophagy in multiple myeloma.Discover oncology · 2025Article
- A translational perspective of the malignant hematopoietic proteoglycome.Cell & bioscience · 2025Review
- CAR T therapies in multiple myeloma: unleashing the future.Cancer gene therapy · 2024Review
- Targeted therapy for multiple myeloma: an overview on CD138-based strategies.Frontiers in oncology · 2024Review
- Global impact of proteoglycan science on human diseases.iScience · 2023Review
- Review
- Eicosanoid regulation of debris-stimulated metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Debris-stimulated tumor growth: a Pandora's box?Cancer metastasis reviews · 2021Review
- Review
- Any closer to successful therapy of multiple myeloma? CAR-T cell is a good reason for optimism.Stem cell research & therapy · 2021Review
- Syndecans and Pancreatic Ductal Adenocarcinoma.Biomolecules · 2021Review
- Syndecan-1 Overexpressing Mesothelioma Cells Inhibit Proliferation, Wound Healing, and Tube Formation of Endothelial Cells.Cancers · 2021Article
- Heparan Sulfate Glycosaminoglycans: (Un)Expected Allies in Cancer Clinical Management.Biomolecules · 2021Review
- 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
- The Role and Therapeutic Value of Syndecan-1 in Cancer Metastasis and Drug Resistance.Frontiers in cell and developmental biology · 2021Review
- Heparanase-enhanced Shedding of Syndecan-1 and Its Role in Driving Disease Pathogenesis and Progression.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Soluble Syndecan-1 Levels Are Associated with Survival in Platinum-Treated Bladder Cancer Patients.Diagnostics (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In patients with multiple myeloma, the heparan sulfate proteoglycan syndecan-1 (CD138) is shed from the surface of tumor cells and accumulates in the serum and within the extracellular matrix of the bone marrow where it promotes tumor growth and metastasis. In the present study we discovered that commonly used anti-myeloma drugs stimulate syndecan-1 shedding both in vitro and in animals bearing myeloma tumors. Enhanced shedding is accompanied by increased syndecan-1 synthesis prior to drug induced tumor cell death. Addition of a caspase inhibitor blocks the drug-induced shedding of syndecan-1 in vitro indicating that shedding is linked to the onset of apoptosis. ADAM inhibitors or siRNA targeting ADAMs blocked drug-induced shedding suggesting that upregulation or activation of ADAMs is responsible for cleaving syndecan-1 from the tumor cell surface. These results reveal that myeloma chemotherapy stimulates synthesis and shedding of syndecan-1, a potentially negative side effect that may lead to the accumulation of high levels of syndecan-1 to establish a microenvironment that nurtures relapse and promotes tumor progression. Interestingly, we also found that chemotherapeutic drugs stimulated syndecan-1 shedding from pancreatic cancer cells as well, indicating that drug-induced shedding of syndecan-1 may occur in many cancer types. Overall, our results indicate that the use of metalloproteinase inhibitors (to inhibit syndecan-1 shedding) in combination with chemotherapy may represent a novel therapeutic strategy to prevent re-establishment of a microenvironment conducive for tumor relapse.
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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.