FOXP3 expression in tumor cells and implications for cancer progression

Tiziana Triulzi, Elda Tagliabue, Andrea Balsari, Patrizia Casalini

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)30-35
Number of pages6
JournalJournal of Cellular Physiology
Issue number1
Publication statusPublished - Jan 2013

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology


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