Abstract
Uveal melanoma (UM) is the most common primary intraocular malignancy and the leading potentially fatal primary intraocular disease in adults. Melanoma antigen recognized by T-cells (MART-1) has been studied extensively as a clinically important diagnostic marker for melanoma, however, its biological function remains unclear. In the present study, the UM cell line SP6.5, which showed a high level of MART-1 expression, was subjected to small interfering RNA-mediated silencing of MART-1. Silencing of MART-1 expression increased the migration ability of SP6.5 cells and down-regulated the expression of the metastasis suppressor NM23. Our results suggest that MART-1 is a candidate target for the development of therapeutic strategies for UM and in particular for the suppression of metastasis associated with this malignancy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Cycle Checkpoints
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Cell Line, Tumor
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Cell Movement
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Cell Proliferation
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Humans
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MART-1 Antigen / chemistry
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MART-1 Antigen / genetics
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MART-1 Antigen / metabolism*
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Melanoma / metabolism
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Melanoma / pathology
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NM23 Nucleoside Diphosphate Kinases / genetics
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NM23 Nucleoside Diphosphate Kinases / metabolism
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RNA Interference*
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RNA, Messenger / metabolism
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RNA, Small Interfering / metabolism
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Tumor Suppressor Proteins / genetics
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Tumor Suppressor Proteins / metabolism
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Ubiquitin Thiolesterase / genetics
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Ubiquitin Thiolesterase / metabolism
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Uveal Melanoma
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Uveal Neoplasms / metabolism
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Uveal Neoplasms / pathology
Substances
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BAP1 protein, human
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MART-1 Antigen
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NM23 Nucleoside Diphosphate Kinases
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RNA, Messenger
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RNA, Small Interfering
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Tumor Suppressor Proteins
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NME1 protein, human
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Ubiquitin Thiolesterase