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Type: Journal article
Title: FOXP3 over-expression inhibits melanoma tumorigenesis via effects on proliferation and apoptosis
Author: Tan, B.
Anaka, M.
Deb, S.
Freyer, C.
Ebert, L.
Chueh, A.
Al-Obaidi, S.
Behren, A.
Jayachandran, A.
Cebon, J.
Chen, W.
Mariadason, J.
Citation: Oncotarget, 2014; 5(1):264-276
Publisher: Impact Journals
Issue Date: 2014
ISSN: 1949-2553
Statement of
BeeShin Tan, Matthew Anaka, Siddhartha Deb, Claudia Freyer, Lisa M. Ebert, Anderly C. Chueh, Sheren Al-Obaidi, Andreas Behren, Aparna Jayachandran, Jonathan Cebon, Weisan Chen and John M. Mariadason
Abstract: The Forkhead box P3 (FOXP3) transcription factor is the key driver of regulatory T cell (Treg cells) differentiation and immunosuppressive function. In addition, FOXP3 has been reported to be expressed in many tumors, including melanoma. However, its role in tumorigenesis is conflicting, with both tumor suppressive and tumor promoting functions described. The aim of the current study was to characterize the expression and function of FOXP3 in melanoma. FOXP3 expression was detected by immunohistochemistry (IHC) in 12% (18/146) of stage III and IV melanomas. However expression was confined to fewer than 1% of cells in these tumors. Stable over-expression of FOXP3 in the SK-MEL-28 melanoma cell line reduced cell proliferation and clonogenicity in vitro, and reduced xenograft growth in vivo. FOXP3 over-expression also increased pigmentation and the rate of apoptosis of SK-MEL-28 cells. Based on its infrequent expression in human melanoma, and its growth inhibitory and pro-apoptotic effect in over-expressing melanoma cells, we conclude that FOXP3 is not likely to be a key tumor suppressor or promoter in melanoma.
Keywords: FOXP3; melanoma; proliferation; apoptosis
Rights: This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
RMID: 0030015661
DOI: 10.18632/oncotarget.1600
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Appears in Collections:Pathology publications

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