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
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Cell Cycle Checkpoints
-
Cell Line, Tumor
-
Cell Movement
-
Cell Proliferation
-
Humans
-
MART-1 Antigen / chemistry
-
MART-1 Antigen / genetics
-
MART-1 Antigen / metabolism*
-
Melanoma / metabolism
-
Melanoma / pathology
-
NM23 Nucleoside Diphosphate Kinases / genetics
-
NM23 Nucleoside Diphosphate Kinases / metabolism
-
RNA Interference*
-
RNA, Messenger / metabolism
-
RNA, Small Interfering / metabolism
-
Tumor Suppressor Proteins / genetics
-
Tumor Suppressor Proteins / metabolism
-
Ubiquitin Thiolesterase / genetics
-
Ubiquitin Thiolesterase / metabolism
-
Uveal Neoplasms / metabolism
-
Uveal Neoplasms / pathology
Substances
-
BAP1 protein, human
-
MART-1 Antigen
-
NM23 Nucleoside Diphosphate Kinases
-
RNA, Messenger
-
RNA, Small Interfering
-
Tumor Suppressor Proteins
-
NME1 protein, human
-
Ubiquitin Thiolesterase