ArticleClinical & experimental metastasis2011
Versican induces a pro-metastatic ovarian cancer cell behavior which can be inhibited by small hyaluronan oligosaccharides.
Article in Clinical & experimental metastasis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Enhanced expression of ADAMTS1 in ovarian carcinomas: loss of ADAMTS1 expression instigates cellular reprogramming of extracellular matrix ensuing altered plasticity, augmented migration and attenuated adhesion.Journal of biomedical science · 2026Article
- Normalizing the Tumor Microenvironment: A New Frontier in Ovarian Cancer Therapy.International journal of molecular sciences · 2026Review
- The protease ADAMTS5 controls ovarian cancer cell invasion, downstream of Rab25.The FEBS journal · 2025Article
- The oncogenic ADAMTS1-VCAN-EGFR cyclic axis drives anoikis resistance and invasion in renal cell carcinoma.Cellular & molecular biology letters · 2024Article
- Cyclic increase in the ADAMTS1-L1CAM-EGFR axis promotes the EMT and cervical lymph node metastasis of oral squamous cell carcinoma.Cell death & disease · 2024Article
- Chemerin Enhances Migration and Invasion of OC Cells via CMKLR1/RhoA/ROCK-Mediated EMT.International journal of endocrinology · 2024Article
- Versican secreted by the ovary links ovulation and migration in fallopian tube derived serous cancer.Cancer letters · 2022Article
- Defining the versican interactome in lung health and disease.American journal of physiology. Cell physiology · 2022Review
- Oxidative damage to hyaluronan-CD44 interactions as an underlying mechanism of action of oxidative stress-inducing cancer therapy.Redox biology · 2021Article
- Hyaluronic Acid: Redefining Its Role.Cells · 2020Review
- The Many Microenvironments of Ovarian Cancer.Advances in experimental medicine and biology · 2020Review
- Targeting the Extra-Cellular Matrix-Tumor Cell Crosstalk for Anti-Cancer Therapy: Emerging Alternatives to Integrin Inhibitors.Frontiers in oncology · 2020Review
- 4-Methylumbelliferone Inhibits Cancer Stem Cell Activation and Overcomes Chemoresistance in Ovarian Cancer.Cancers · 2019Article
- Molecular Mechanisms Regulating Organ-Specific Metastases in Epithelial Ovarian Carcinoma.Cancers · 2018Review
- Cancer Cell Glycocalyx and Its Significance in Cancer Progression.International journal of molecular sciences · 2018Review
- Charting the unexplored extracellular matrix in cancer.International journal of experimental pathology · 2018Review
- Effects of anti-CD44 monoclonal antibody IM7 carried with chitosan polylactic acid-coated nano-particles on the treatment of ovarian cancer.Oncology letters · 2017Article
- Probing chromatin landscape reveals roles of endocardial TBX20 in septation.The Journal of clinical investigation · 2016Article
- Versican and vascular endothelial growth factor expression levels in peritoneal metastases from colorectal cancer are associated with survival after cytoreductive surgery and hyperthermic intraperitoneal chemotherapy.Clinical & experimental metastasis · 2016Article
- The Importance of CD44 as a Stem Cell Biomarker and Therapeutic Target in Cancer.Stem cells international · 2016Review
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5 authors.
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Abstract
The assembly of pericellular matrix containing hyaluronan (HA) and versican has been shown to be a pre-requisite for proliferation and migration of mesenchymal cells. In this study, we investigated whether treatment with recombinant versican could induce the formation of a pericellular matrix by ovarian cancer cells (OVCAR-3, OVCAR-5, and SKOV-3) and promote their motility, invasion, and adhesion to peritoneal cells in vitro. We also determined whether versican-induced pericellular matrix formation and metastatic cancer cell behavior could be blocked by small HA oligosaccharides. Only combined treatment with recombinant versican and HA resulted in pericellular matrix formation by OVCAR-5 and SKOV-3 but not by OVCAR-3 cells, which lack the HA receptor, CD44. The motility of OVCAR-5 and SKOV-3 cells was significantly increased in scratch wound and chemotaxis assays following treatment with recombinant versican and HA. Versican and HA also promoted invasion of SKOV-3 and OVCAR-5 cells but had no effect on OVCAR-3 cells. We have demonstrated that exogenous HA significantly increased OVCAR-5 and SKOV-3 adhesion to peritoneal cells but adhesion was not further increased by versican treatment. Small HA oligomers (6-10 disaccharides) were able to significantly block formation of pericellular matrix by OVCAR-5 cells, as well as the increased motility and invasion induced by recombinant versican. HA oligomers also significantly blocked OVCAR-5 adhesion to peritoneal cells both in the presence and absence of exogenous HA. The dependence of CD44 for the versican and HA mediated effects were demonstrated by the inhibition of pericellular matrix formation as well as motility and invasion of OVCAR-5 cells following treatment with CD44 neutralizing antibody in the presence of versican and HA. We conclude that the acquisition of a HA/versican pericellular matrix by ovarian cancer cells increases their metastatic potential. HA oligomers can block this mechanism and are promising inhibitors of ovarian cancer dissemination.
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