Cytokine-mediated modulation of integrin, ICAM-1 and CD44 expression on human uveal melanoma cells in vitro

Creyghton, W.M.; Waard-Siebinga, I. de; Danen, Erik H.J.; Luyten, Gré P.M.; Muijen, G.N.P. van; Jager, M. J.

doi:10.1097/00008390-199508000-00005

Cited by 23 publications

(12 citation statements)

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“…Available data suggest that the expression of ICAM-1 and integrins on melanoma cells is up-regulated in response to various cytokines, including interferon (IFN)-g, IL-1 and TNF-a [50][51][52], and other stresses such as sublethal laser radiation [53]. In the present study, we evaluated the impact of single and combined exposures to serotonin and ionizing radiation on the cell surface expression of ICAM-1 and integrins beta1, alpha2, alpha5 and alpha6 on IPC-298 melanoma cells.…”

Section: Discussionmentioning

confidence: 99%

Serotonin and ionizing radiation synergistically affect proliferation and adhesion molecule expression of malignant melanoma cells

Müller

Gilbertz

Meineke

2012

Journal of Dermatological Science

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Section: Discussionmentioning

confidence: 99%

Serotonin and ionizing radiation synergistically affect proliferation and adhesion molecule expression of malignant melanoma cells

Müller

Gilbertz

Meineke

2012

Journal of Dermatological Science

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“…Several papers have shown that type I and type II IFNs can have variable effects on cell proliferation and integrin/adhesion molecule expression in uveal melanoma (12,13). Like cutaneous melanoma, the biology of uveal melanoma can also be affected through decitabine-induced gene re-expression.…”

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confidence: 99%

Decitabine Up-regulates S100A2 Expression and Synergizes with IFN-γ to Kill Uveal Melanoma Cells

Gollob

Sciambi

2007

Clinical Cancer Research

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Purpose: Metastatic uveal melanoma is resistant to conventional chemotherapy and immunotherapy. In this study, we investigated the responsiveness of uveal melanoma cell lines to IFNs and the hypomethylating agent decitabine. Experimental Design: The uveal melanoma cell lines 92-1, UW-1, OCM-1, and MKT-BR were exposed to varying concentrations of IFN-a, IFN-g, and decitabine, alone and in combination. The effects of decitabine on gene expression were examined using DNA microarray analysis. Results: We found that IFN-g and decitabine induced cell death in uveal melanoma. Whereas a high concentration of IFN-g (1,000 units/mL) was required to induce cell death, we observed a dose-related increase in cell death when decitabine was used at a range of 0.1 to 10 Amol/L. Strikingly, 1 Amol/L decitabine synergized with 10 to 1,000 units/mL IFN-g to induce massive cell death. In contrast, decitabine had no effect on three cutaneous melanoma cell lines and exhibited no synergy with either IFN. In uveal melanoma, decitabine up-regulated the expression of genes involved in growth control and apoptosis and down-regulated genes that have been implicated in the malignant phenotype of cutaneous melanoma. The gene up-regulated to the greatest degree by decitabine and whose expression showed a dose-effect across the three concentrations of decitabine was S100A2, a putative tumor suppressor.The genes modulated by decitabine in uveal melanoma were largely unaffected in cutaneous melanoma. Conclusions: These findings form a basis for testing the decitabine/IFN-g combination in metastatic uveal melanoma and for exploring the role of S100A2 in the susceptibility of uveal melanoma to IFN-mediated cell death.Metastatic uveal melanoma is an aggressive malignancy with a median survival of <6 months (1). Patients with locally advanced primary lesions also have a poor prognosis because up to 50% will subsequently develop disseminated metastases within 10 years (2). Although hepatic metastases can respond partially to intra-arterial chemotherapy or chemoembolization, metastatic uveal melanoma is largely resistant to systemic chemotherapy (3). Immunomodulatory drugs used to treat advanced cutaneous melanoma, including interleukin 2 (IL-2) and IFN-a, have also had very limited activity in uveal melanoma (4).The mechanism underlying the antitumor effect of IFN-a or IL-2 in select patients with advanced cutaneous melanoma remains poorly defined. The association of good outcome with the development of autoimmune breakthrough events (5,6) suggests that overcoming tolerance to self-antigens plays a role in cytokine-mediated antitumor immunity. However, IFN-a and IFN-g can also exert direct antiproliferative and/or proapoptotic effects on cutaneous melanoma cell lines (7, 8), illustrating how certain cytokines can have antitumor effects that are independent of the induction of antigen-specific cellular or humoral immunity.The epigenetic suppression of gene expression through DNA methylation has been linked to the relative resistance of a cuta...

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“…Changes in the expression of cellular adhesion molecules (Hynes, 1992;Natali et al, 1993;Danen et al, 1995;Stuiver and O'Toole, 1995) and matrix metalloproteinase activity (Hojo et al, 2002) are strongly associated with an increase in melanoma phenotype and invasion. Of particular note is that integrin and adhesion molecule expression can be directly upregulated by proinflammatory cytokines within the local cellular environment (Creyghton et al, 1995).…”

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confidence: 99%

Melanoma cell migration is upregulated by tumour necrosis factor-α and suppressed by α-melanocyte-stimulating hormone

et al. 2004

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We reported recently that the inflammatory cytokine tumour necrosis factor a (TNF-a) can upregulate integrin expression, cell attachment and invasion of cells through fibronectin in a human melanoma cell line (HBL). Furthermore, the actions of TNF-a were suppressed by the addition of an anti-inflammatory peptide a-melanocyte-stimulating hormone (a-MSH). In the current study, we extend this work investigating to what extent TNF-a might stimulate melanoma invasion by promoting cell migration and whether a-MSH is also inhibitory. Two human melanoma cell lines were examined in vitro (HBL and C8161) using a scratch migration assay. Analysis using either time-lapse video microscopy or imaging software analysis of migrating 'fronts' of cells revealed that C8161 cells migrated more rapidly than HBL cells. However, when cells were stimulated with TNF-a both cell types responded with a significant increase in migration distance over a 16 -26 h incubation time. a-Melanocyte-stimulating hormone had an inhibitory effect on TNF-astimulated migration for HBL cells, completely blocking migration at 10 À9 M. In contrast, C8161 cells did not respond to a-MSH (as these cells have a loss-of-function melanocortin-1 receptor). However, stable transfection of C8161 cells with the wild-type melanocortin-1 receptor produced cells whose migration was significantly inhibited by a-MSH. In addition, the use of a neutralising antibody to the b 1 -integrin subunit significantly reduced migration in both cell types. This data therefore supports an inflammatory environment promoting melanoma cell migration, and in addition shows that a-MSH can inhibit inflammatory stimulated migration. The data also support a fundamental role of the b 1 -integrin receptor in melanoma cell migration.

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Cytokine-mediated modulation of integrin, ICAM-1 and CD44 expression on human uveal melanoma cells in vitro

Cited by 23 publications

References 0 publications

Serotonin and ionizing radiation synergistically affect proliferation and adhesion molecule expression of malignant melanoma cells

Serotonin and ionizing radiation synergistically affect proliferation and adhesion molecule expression of malignant melanoma cells

Decitabine Up-regulates S100A2 Expression and Synergizes with IFN-γ to Kill Uveal Melanoma Cells

Melanoma cell migration is upregulated by tumour necrosis factor-α and suppressed by α-melanocyte-stimulating hormone

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