ArticleThe Journal of biological chemistry2011
V3 versican isoform alters the behavior of human melanoma cells by interfering with CD44/ErbB-dependent signaling.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- V3: an enigmatic isoform of the proteoglycan versican.American journal of physiology. Cell physiology · 2023Review
- Defining the versican interactome in lung health and disease.American journal of physiology. Cell physiology · 2022Review
- Proteoglycans in Cancer: Friends or Enemies? A Special Focus on Hepatocellular Carcinoma.Cancers · 2022Review
- Time-Resolved Extracellular Matrix Atlas of the Developing Human Skin Dermis.Frontiers in cell and developmental biology · 2021Article
- Interplay between Cell-Surface Receptors and Extracellular Matrix in Skin.Biomolecules · 2020Review
- The synthesis and secretion of versican isoform V3 by mammalian cells: A role for N-linked glycosylation.Matrix biology : journal of the International Society for Matrix Biology · 2020Article
- Versican-A Critical Extracellular Matrix Regulator of Immunity and Inflammation.Frontiers in immunology · 2020Review
- Decline in arylsulfatase B expression increases EGFR expression by inhibiting the protein-tyrosine phosphatase SHP2 and activating JNK in prostate cells.The Journal of biological chemistry · 2018Article
- Proteoglycans as Immunomodulators of the Innate Immune Response to Lung Infection.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Review
- HER-2 and EGFR mRNA Expression and Its Relationship with Versican in Malignant Matrix-Producing Tumors of the Canine Mammary Gland.PloS one · 2016Article
- Expression of V3 Versican by Rat Arterial Smooth Muscle Cells Promotes Differentiated and Anti-inflammatory Phenotypes.The Journal of biological chemistry · 2015Article
- Proteoglycans in Normal and Healing Skin.Advances in wound care · 2015Article
- Versican and the regulation of cell phenotype in disease.Biochimica et biophysica acta · 2014Review
- Expression of versican V3 by arterial smooth muscle cells alters tumor growth factor β (TGFβ)-, epidermal growth factor (EGF)-, and nuclear factor κB (NFκB)-dependent signaling pathways, creating a microenvironment that resists monocyte adhesion.The Journal of biological chemistry · 2014Article
- Versican and the control of inflammation.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
- Arylsulfatase B (N-acetylgalactosamine-4-sulfatase): potential role as a biomarker in prostate cancer.Prostate cancer and prostatic diseases · 2013Article
- Proteoglycans and their roles in brain cancer.The FEBS journal · 2013Review
- An introduction to proteoglycans and their localization.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012Review
- Hyaluronan and versican in the control of human T-lymphocyte adhesion and migration.Matrix biology : journal of the International Society for Matrix Biology · 2012Article
- Antithetic roles of proteoglycans in cancer.Cellular and molecular life sciences : CMLS · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Versican is a hyaluronan-binding, extracellular chondroitin sulfate proteoglycan produced by several tumor types, including malignant melanoma, which exists as four different splice variants. The short V3 isoform contains the G1 and G3 terminal domains of versican that may potentially interact directly or indirectly with the hyaluronan receptor CD44 and the EGFR, respectively. We have previously described that overexpression of V3 in MeWo human melanoma cells markedly reduces tumor cell growth in vitro and in vivo. In this study we have investigated the signaling mechanism of V3 by silencing the expression of CD44 in control and V3-expressing melanoma cells. Suppression of CD44 had the same effects on cell proliferation and cell migration than those provoked by V3 expression, suggesting that V3 acts through a CD44-mediated mechanism. Furthermore, CD44-dependent hyaluronan internalization was blocked by V3 expression and CD44 silencing, leading to an accumulation of this glycosaminoglycan in the pericellular matrix and to changes in cell migration on hyaluronan. Furthermore, ERK1/2 and p38 activation after EGF treatment were decreased in V3-expressing cells suggesting that V3 may also interact with the EGFR through its G3 domain. The existence of a EGFR/ErbB2 receptor complex able to interact with CD44 was identified in MeWo melanoma cells. V3 overexpression resulted in a reduced interaction between EGFR/ErbB2 and CD44 in response to EGF treatment. Our results indicate that the V3 isoform of versican interferes with CD44 and the CD44-EGFR/ErbB2 interaction, altering the signaling pathways, such as ERK1/2 and p38 MAPK, that regulate cell proliferation and migration.
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