P63 is a suppressor of tumorigenesis and metastasis interacting with mutant p53

Research output: Contribution to journalArticle

148 Citations (Scopus)

Abstract

p53 mutations, occurring in two-thirds of all human cancers, confer a gain of function phenotype, including the ability to form metastasis, the determining feature in the prognosis of most human cancer. This effect seems mediated at least partially by its ability to physically interact with p63, thus affecting a cell invasion pathway, and accordingly, p63 is deregulated in human cancers. In addition, p63, as an epithelial organizer, directly impinges on epidermal mesenchimal transition, stemness, senescence, cell death and cell cycle arrest, all determinant in cancer, and thus p63 affects chemosensitivity and chemoresistance. This demonstrates an important role for p63 in cancer development and its progression, and the aim of this review is to set this new evidence that links p63 to metastasis within the context of the long conserved other functions of p63.

Original languageEnglish
Pages (from-to)1487-1499
Number of pages13
JournalCell Death and Differentiation
Volume18
Issue number9
DOIs
Publication statusPublished - Sep 2011

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Carcinogenesis
Neoplasm Metastasis
Neoplasms
Cell Cycle Checkpoints
Cell Death
Phenotype
Mutation

Keywords

  • cancer
  • metastasis
  • p53
  • p63
  • p73
  • tumor suppressor

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

P63 is a suppressor of tumorigenesis and metastasis interacting with mutant p53. / Melino, G.

In: Cell Death and Differentiation, Vol. 18, No. 9, 09.2011, p. 1487-1499.

Research output: Contribution to journalArticle

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