Role of Fas ligand in uveal melanoma-induced liver damage

Repp, Amanda C.; Mayhew, Elizabeth; Howard, Kevin; Alizadeh, Hassan; Niederkorn, Jérry Y.

doi:10.1007/s004170100363

Cited by 11 publications

(5 citation statements)

References 24 publications

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“…More precise understanding of the molecular pathogenesis of uveal melanoma is re q u i red for the development of alternative therapies. Recent results, including ours, indicate pro g ress in this field (4)(5)(6)(7).…”

Section: Introductionsupporting

confidence: 53%

“…To measure the cell viability 5x10 5 OCM-1 cells were seeded into 24 well-plates. Cells were cultured for 6 hours in 1 mL of medium, as described above, and then treated with various concentrations of s 4 U M P. One h u n d red µL aliquots were removed in triplicate at the indicated time for MTT [3-(4,5-dimethylthiazolyl-2)-2, 5-diphenyl-tetrazolium bromide] assay.…”

Section: Mtt Assaymentioning

confidence: 99%

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Antiproliferative Effect of 4-Thiouridylate on OCM-1 Uveal Melanoma Cells

Kemény-Beke

Berényi

Facskó

et al. 2006

European Journal of Ophthalmology

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Section: Introductionsupporting

confidence: 53%

Section: Mtt Assaymentioning

confidence: 99%

Antiproliferative Effect of 4-Thiouridylate on OCM-1 Uveal Melanoma Cells

Kemény-Beke

Berényi

Facskó

et al. 2006

European Journal of Ophthalmology

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“…Alternatively, secretion of processed "soluble" FasL [6] or FasL-bearing microvesicles [7] by cancer cells may create a specific shield, which allows them to dampen the effects of cytotoxic lymphocytes or natural killer cells. A role of endogenous FasL expression in the "tumor counterattack" hypothesis is still under active investigation [3,8,9]; however, experimental data certainly demonstrated FasL expression in some cancer cell lines, including melanomas [6,7,10,11]. Taken together, these observations illustrate important aspects of the general problem of the resistance of cancer cells to the induction of programmed cell death.…”

Section: Introductionmentioning

confidence: 99%

Dual treatment with COX-2 inhibitor and sodium arsenite leads to induction of surface Fas Ligand expression and Fas-Ligand-mediated apoptosis in human melanoma cells

Ivanov¹,

Hei²

2006

Experimental Cell Research

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Most human melanomas express Fas receptor on the cell surface, and treatment with exogenous Fas Ligand (FasL) efficiently induces apoptosis of these cells. In contrast, endogenous surface expression of FasL is suppressed in Fas-positive melanomas. We report here the use of a combination of sodium arsenite, an inhibitor of NF-κB activation, and NS398, a cyclooxygenase-2 (COX-2) inhibitor, for restoration of the surface FasL expression. We observed a large increase of Fas-mediated apoptosis in Fas-positive melanomas. This was due to induction of FasL surface expression and increased susceptibility to Fas death signaling after arsenite and NS398 treatment. Furthermore, silencing COX-2 expression by specific RNAi also effectively increased surface FasL expression following arsenite treatment. Upregulation of the surface FasL levels was based on an increase in the efficiency of translocation to the cell surface and stabilization of FasL protein on the cell surface, rather than on acceleration of the FasL gene transcription. Data obtained demonstrate that the combination of arsenite with inhibitors of COX-2 may affect the target cancer cells via induction of FasL-mediated death signaling.

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“…Expression of FasL on ocular tissues plays a crucial role in corneal allograft survival by apoptosis of effector T cells [17]. In addition to direct FasL expression on UM [18], UM secretes soluble FasL to inhibit cytotoxic T-cell mediated tumor lysis [19]. The expression Immunotherapy for uveal melanoma review future science group www.futuremedicine.com of inhibitory molecules such as PD-L1 and FasL on both ocular cells and UM may contribute to tumor development and progression by suppression of antitumor immunity.…”

Section: Immunobiology Of the Eye And Ummentioning

confidence: 99%

Immunotherapy for Uveal Melanoma

2016

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Uveal melanoma (UM) is a rare cancer with a high mortality rate. In comparison to cutaneous melanoma, UM has unique immunological features. Arising in the immune suppressive environment of the eye, it maintains immune resistance once metastatic. This is considered a major obstacle for successful immunotherapy in UM. However, a growing body of evidence suggests strategies that may abrogate resistance and enhance antitumor immunity in UM. Recently, three new immune agents have been approved for melanoma. While these drugs demonstrate durable clinical responses with long-term remissions in metastatic cutaneous melanoma, only limited data exist in metastatic UM. In this review, immunological aspects of UM and data from clinical studies of immunotherapeutic agents and regimens for UM will be discussed.

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Role of Fas ligand in uveal melanoma-induced liver damage

Abstract: FasL-induced apoptosis of hepatocytes in contact with FasL-positive human uveal melanoma cells may contribute to hepatic failure during metastatic disease.

Cited by 11 publications

References 24 publications

Antiproliferative Effect of 4-Thiouridylate on OCM-1 Uveal Melanoma Cells

Antiproliferative Effect of 4-Thiouridylate on OCM-1 Uveal Melanoma Cells

Dual treatment with COX-2 inhibitor and sodium arsenite leads to induction of surface Fas Ligand expression and Fas-Ligand-mediated apoptosis in human melanoma cells

Immunotherapy for Uveal Melanoma

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