The DOI matches its Crossref record; 115 of the 115 references it cites were found in a registry or an index.
The heparanase/syndecan‐1 axis in cancer: mechanisms and therapies
Open accessAbstract
Heparanase is an endoglucuronidase that cleaves heparan sulfate chains of proteoglycans. In many malignancies, high heparanase expression and activity correlate with an aggressive tumour phenotype. A major consequence of heparanase action in cancer is a robust up‐regulation of growth factor expression and increased shedding of syndecan‐1 (a transmembrane heparan sulfate proteoglycan). Substantial evidence indicates that heparanase and syndecan‐1 work together to drive growth factor signalling and regulate cell behaviours that enhance tumour growth, dissemination, angiogenesis and osteolysis. Preclinical and clinical studies have demonstrated that therapies targeting the heparanase/syndecan‐1 axis hold promise for blocking the aggressive behaviour of cancer.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“A number of preclinical and clinical findings have reported that targeting pathways and molecules involved in the formation of exosome can inhibit tumor progression, such as heparanase/syndecan-1 axis [182, 183] or syndecan heparan sulfate proteoglycans [179, 184].”
From Tumor microenvironment complexity and therapeutic implications at a glance (2020) · cites this paper as [182]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Valadi, H., Ekström, K., Bossios, A., Sjöstrand, M., Lee, J. J., & Lötvall, J. O. (2007) · Nature Cell Biology · doi:10.1038/ncb1596 · Cited by 12,834
Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET
Peinado, H., Alečković, M., Lavotshkin, S., Matei, I., Costa-Silva, B., Moreno-Bueno, G., Hergueta-Redondo, M., Williams, C., García-Santos, G., Ghajar, C. M., et al. (2012) · Nature Medicine · doi:10.1038/nm.2753 · Cited by 3,715
Requirement of Vascular Integrin α v β 3 for Angiogenesis
Brooks, P. C., Clark, R. A. F., & Cheresh, D. A. (1994) · Science · doi:10.1126/science.7512751 · Cited by 3,020
Functions of Cell Surface Heparan Sulfate Proteoglycans
Bernfield, M. R., Götte, M., Park, P. W., Reizes, O., Fitzgerald, M. L., Lincecum, J. M., & Zako, M. (1999) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.68.1.729 · Cited by 2,722
Met, metastasis, motility and more
Birchmeier, C., Birchmeier, W., Gherardi, E., & Woude, G. F. V. (2003) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1261 · Cited by 2,652
Syndecan–syntenin–ALIX regulates the biogenesis of exosomes
Baietti, M. F., Zhang, Z., Mortier, E., Melchior, A., Degeest, G., Geeraerts, A., Ivarsson, Y., Depoortere, F., Coomans, C., Vermeiren, E., et al. (2012) · Nature Cell Biology · doi:10.1038/ncb2502 · Cited by 1,899
Exosome Secretion: Molecular Mechanisms and Roles in Immune Responses
Bobrie, A., Colombo, M., Raposo, G., & Théry, C. (2011) · Traffic · doi:10.1111/j.1600-0854.2011.01225.x · Cited by 1,148
Schmidt, E. P., Yang, Y., Janssen, W. J., Gandjeva, A., Perez, M. J., Barthel, L., Zemans, R. L., Bowman, J. C., Koyanagi, D., Yunt, Z. X., et al. (2012) · Nature Medicine · doi:10.1038/nm.2843 · Cited by 842
Microvesicles derived from activated platelets induce metastasis and angiogenesis in lung cancer
Janowska‐Wieczorek, A., Wysoczynski, M., Kijowski, J., Marquez‐Curtis, L. A., Machaliński, B., Ratajczak, J., & Ratajczak, M. Z. (2004) · International Journal of Cancer · doi:10.1002/ijc.20657 · Cited by 781
Large-scale proteomics and phosphoproteomics of urinary exosomes
Gonzales, P. A., Pisitkun, T., Hoffert, J. D., Tchapyjnikov, D., Star, R. A., Kleta, R., Wang, N. S., & Knepper, M. A. (2009) · Journal of the American Society of Nephrology · doi:10.1681/asn.2008040406 · Cited by 727
Research works printed but not linked: 1
- 10.1042/0264-6021:3370471 · DOI
Cited by
Sorted by citations
Extracellular matrix structure
Theocharis, A. D., Skandalis, S. S., Gialeli, C., & Karamanos, N. K. (2016) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2015.11.001 · Cited by 2,598
Tumor microenvironment complexity and therapeutic implications at a glance
Baghban, R., Roshangar, L., Jahanban-Esfahlan, R., Seidi, K., Ebrahimi-Kalan, A., Jaymand, M., Kolahian, S., Javaheri, T., & Zare, P. (2020) · Cell Communication and Signaling · doi:10.1186/s12964-020-0530-4 · Cited by 1,784
“A number of preclinical and clinical findings have reported that targeting pathways and molecules involved in the formation of exosome can inhibit tumor progression, such as heparanase/syndecan-1 axis [182, 183] or syndecan heparan sulfate proteoglycans [179, 184] .”
BackgroundYuan, Z., Li, Y., Zhang, S., Wang, X., Dou, H., Yu, X., Zhang, Z., Yang, S., & Xiao, M. (2023) · Molecular Cancer · doi:10.1186/s12943-023-01744-8 · Cited by 977
Syn, N. L. X., Wang, L., Sethi, G., Thiery, J. P., & Goh, B. C. (2016) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2016.04.006 · Cited by 484
TIMPs: versatile extracellular regulators in cancer
Jackson, H. W., Defamie, V., Waterhouse, P. D., & Khokha, R. (2016) · Nature reviews. Cancer · doi:10.1038/nrc.2016.115 · Cited by 454
Metadata
- Authors
- Ramani, V. C., Purushothaman, A., Stewart, M. D., Thompson, C. A., Vlodavsky, I., Au, J. L., & Sanderson, R. D.
- Affiliations
- University of Alabama at Birmingham (US)
- Cancer and Vascular Biology Research Center Rappaport Faculty of Medicine Haifa Israel
- Optimum Therapeutics (United States) (US)
- Corresponding author
- Sanderson, Ralph D.
- Venue
- The FEBS Journal
- Publisher
- Wiley
- Published
- 2013-03-04
- Volume
- 280
- Issue
- 10
- Pages
- 2294-2306
- ISSN
- 1742-464X (ISSN-L)
- 1742-4658
- PMC
- PMC3651779
- OpenAlex
- W2104368170
- Cited by
- 189
- References
- 115
- Citations by year
- 2026: 7 · 2025: 2 · 2024: 5 · 2023: 9 · 2022: 16 · 2021: 17 · 2020: 18 · 2019: 8 · 2018: 12 · 2017: 11 · 2016: 30 · 2015: 21 · 2014: 24 · 2013: 9
- FWCI
- 3.22
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- FEBS Journal (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (CA135075, CA138340, R01CA138340, CA138535, R01CA135075, R01CA138535)
- National Institute of General Medical Sciences (T32GM008111)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- heparanase, syndecan-1, heparan sulfate proteoglycans, cancer, growth factor signaling, tumor growth, metastasis, angiogenesis, osteolysis, heparanase inhibitors
- MeSH terms
- Heparanase, Animals, Antineoplastic Agents, Cell Nucleus, Enzyme Activation, Enzyme Inhibitors, Glucuronidase, Heparitin Sulfate, Heparan Sulfate, Humans, Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Hepatocyte Growth Factor, Biomimetic Materials, Syndecan-1, Exosomes
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
