Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 228, Issue 1, Pages 30-35Publisher
WILEY-BLACKWELL
DOI: 10.1002/jcp.24125
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Funding
- AIRC
- Italian Bureau of Health
- Associazione Italiana per la Ricerca sul Cancro (AIRC)
- Italian Bureau of Health (Alleanza contro il Cancro)
- Italian government
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FOXP3 is a member of the forkhead/winged-helix family of transcriptional regulators. Defects in the FOXP3 gene cause an X-linked autoimmune/immunodeficiency syndrome in humans and the Scurfy phenotype in mice. FOXP3 acts mainly in regulating the development and function of CD4+CD25+ regulatory T cells. Although initially thought to be specific for these cells, FOXP3 expression has recently been described in non-hematopoietic cells, including epithelial cells of multiple lineages and of different tissue origins. Moreover, FOXP3 expression has been detected in tumor cells of both epithelial and non-epithelial tissues. The role of FOXP3 expression by tumor cells remains controversial, with in vitro studies pointing to an onco-suppressive action, whereas studies conducted on human samples associate FOXP3 expression by tumor cells with metastatic spread. Here, we review evidence for the multi-faceted role of FOXP3 in cancer cells. J. Cell. Physiol. 228: 3035, 2013. (c) 2012 Wiley Periodicals, Inc.
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