Versican Is Differentially Expressed in Human Melanoma and May Play a Role in Tumor Development

Touab, Malika; Villena, Juan; Barranco, Carlos; Arumí-Uría, Montserrat; Bassols, Anna

doi:10.1016/s0002-9440(10)64874-2

Cited by 113 publications

(126 citation statements)

References 31 publications

(31 reference statements)

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“…Versican expression was normalized against a household gene (EEF1A1). 12,13,[16][17][18]20,23,34,[36][37][38][39] As the composition of the ECM influences the migration of inflammatory cells, 33 we have also measured the association between inflammatory cells and versican expression. Despite the reported production of versican isoforms V0 and V1 by human leukemic monocytes 40 and the reported …”

Section: Discussionmentioning

confidence: 99%

“…10,15 Indeed, increased levels of versican have been reported in different tumor types such as adenocarcinomas, [16][17][18] squamous cell carcinomas, 19,20 sarcomas, 21 mesotheliomas 22 and malignant melanomas. 23 In addition, versican expression has been associated with tumor progression and decreased survival in various tumor types. [24][25][26] In cervical cancer, versican has been suggested to enhance tumor invasion and metastases formation.…”

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confidence: 99%

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Versican expression is associated with tumor-infiltrating CD8-positive T cells and infiltration depth in cervical cancer

et al. 2010

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Cervical carcinoma is the second most frequent cancer type in women worldwide. Both inflammatory cells and stromal cells are important for tumor progression. Stromal cells produce growth factors and extracellular matrix and provide an adequate environment for angiogenesis. Versican, a member of the extracellular matrix, has been shown to have a role in tumor progression. The aim of this study was to investigate versican expression, and its association with tumor-infiltrating inflammatory cell subsets and with clinicopathological parameters in human cervical cancers. We have studied the expression of versican in 149 cervical cancers using immunohistochemistry and mRNA in situ hybridization. Versican was predominantly expressed in the stroma (myofibroblasts). Using quantitative real-time-PCR, V0 was found to be the most prominent isoform. High stromal versican expression was significantly associated with a low number of tumor-infiltrating T cells (P ¼ 0.018) and particularly a low number of CD8-positive T cells (cytotoxic T cells; P ¼ 0.002). Stromal versican expression was significantly higher in patients with an infiltration depth 414 mm (P ¼ 0.004) and in patients with parametrial invasion (P ¼ 0.044). Stromal versican expression was not associated with survival. Our results suggest that versican expression in the stromal compartment of cervical cancers results in reduced numbers of intraepithelial CD8-positive T cells and enhanced local invasion.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Versican expression is associated with tumor-infiltrating CD8-positive T cells and infiltration depth in cervical cancer

et al. 2010

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“…The largest splice variants of versican, V0 and V1, are the predominant forms present in most glioma cell lines, whereas V2 is rarely expressed, consistent with previous studies concerning human glioma cell lines (Dours-Zimmermann and Zimmermann, 1994;Bouterfa et al, 1999). Expression of V0/V1 isoforms increases in different tumours (Touab et al, 2002), suggesting that these isoforms may be involved in tumour development. In this context, our results show that V0/V1 are the main versican isoforms related to the malignant phenotype of glioma in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…Versican-rich extracellular matrices exert an anti-adhesive effect on the tumour cells (Yamagata and Kimata, 1994;Touab et al, 2002), thus facilitating tumour cell migration and invasion. It has was analysed in spheroid assays as described in methods.…”

Section: Discussionmentioning

confidence: 99%

The role of versican isoforms V0/V1 in glioma migration mediated by transforming growth factor-β2

et al. 2007

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Versican is a large chondroitin sulphate proteoglycan produced by several tumour cell types, including high-grade glioma. The increased expression of certain versican isoforms in the extracellular matrix (ECM) plays a role in tumour cell growth, adhesion and migration. Transforming growth factor-b2 (TGF-b2) is an important modulator of glioma invasion, partially by remodeling the ECM. However, it is unknown whether it interacts with versican during malignant progression of glioma cells. Here, we analysed the effect of TGF-b2 on the expression of versican isoforms. The expression of versican V0/V1 was upregulated by TGF-b2 detected by quantitative polymerase chain reaction and immunoprecipitation, whereas V2 was not induced. Using time-lapse scratch and spheroid migration assays, we observed that the glioma migration rate is significantly increased by exogenous TGF-b2 and inhibited by TGF-b2-specific antisense oligonucleotides. Interestingly, an antibody specific for the DPEAAE region of glycosaminoglycan-b domain of versican was able to reverse the effect of TGF-b2 on glioma migration in a dose-dependent manner. Taken together, we report here that TGF-b2 triggers the malignant phenotype of high-grade gliomas by induction of migration, and that this effect is, at least in part, mediated by versican V0/V1.

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“…Studies have shown versican to interact with fibronectin, as well as collagen type I [67] and that these interactions are responsible for reduced cell adhesion in melanoma cells [68]. Fibronectin and collagen are integrin ligands and play roles in enhancing cell adhesion.…”

Section: Versican Interaction With Fibronectinmentioning

confidence: 99%

The interaction of versican with its binding partners

et al. 2005

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Versican belongs to the family of the large aggregating chondroitin sulfate proteoglycans located primarily within the extracellular matrix (ECM). Versican, like other members of its family, has unique N-and C-terminal globular regions, each with multiple motifs. A large glycosaminoglycan-binding region lies between them. This review will begin by outlining these structures, in the context of ECM proteoglycans. The diverse binding partners afforded to versican by virtue of its modular design will then be examined. These include ECM components, such as hyaluronan, type I collagen, tenascin-R, fibulin-1, and -2, fibrillin-1, fibronectin, P-and L-selectins, and chemokines. Versican also binds to the cell surface proteins CD44, integrin β1, epidermal growth factor receptor, and P-selectin glycoprotein ligand-1. These multiple interactors play important roles in cell behaviour, and the roles of versican in modulating such processes are discussed.

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Versican Is Differentially Expressed in Human Melanoma and May Play a Role in Tumor Development

Cited by 113 publications

References 31 publications

Versican expression is associated with tumor-infiltrating CD8-positive T cells and infiltration depth in cervical cancer

Versican expression is associated with tumor-infiltrating CD8-positive T cells and infiltration depth in cervical cancer

The role of versican isoforms V0/V1 in glioma migration mediated by transforming growth factor-β2

The interaction of versican with its binding partners

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