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Int. J. Mol. Sci. 2013, 14(7), 15092-15104; doi:10.3390/ijms140715092
Article

Targeted Silencing of MART-1 Gene Expression by RNA Interference Enhances the Migration Ability of Uveal Melanoma Cells

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1,*  and 1,*
1 Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China 2 Department of Clinical Laboratories, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China These authors contributed equally to this work.
* Authors to whom correspondence should be addressed.
Received: 15 May 2013 / Revised: 11 July 2013 / Accepted: 15 July 2013 / Published: 19 July 2013
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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.
Keywords: uveal melanoma; MART-1; NM23; migration ability uveal melanoma; MART-1; NM23; migration ability
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Zhang, Y.; Jia, R.; Wang, J.; Xu, X.; Yao, Y.; Ge, S.; Fan, X. Targeted Silencing of MART-1 Gene Expression by RNA Interference Enhances the Migration Ability of Uveal Melanoma Cells. Int. J. Mol. Sci. 2013, 14, 15092-15104.

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