Mechanisms, function and clinical applications of DNp73

Cell Cycle. 2013 Jun 15;12(12):1861-7. doi: 10.4161/cc.24967. Epub 2013 Jun 13.

Abstract

p73, has two distinct promoters, which allow the formation of two protein isoforms: full-length transactivating (TA) p73 and an N-terminally truncated p73 species (referred to as DNp73) that lacks the N-terminal transactivating domain. Although the exact cellular function of DNp73 is unclear, the high expression levels of the genes have been observed in a variety of human cancers and cancer cell lines and have been connected to pro-tumor activities. Hence the aim of this review is to summarize DNp73 expression status in cancer in the current literature. Furthermore, we also focused on recent findings of DNp73 related to the biological functions from apoptosis, chemosensitivity, radiosensitibity, differentiation, development, etc. Thus this review highlights the significance of DNp73 as a marker for disease severity in patients and as target for cancer therapy.

Keywords: DNp73; alternative splicing; apoptosis; cancer; chemosensitivity; radiotherapy; tumorigenesis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Apoptosis / physiology
  • Cell Differentiation / genetics
  • Cell Differentiation / physiology
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Humans
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Tumor Protein p73
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*

Substances

  • DNA-Binding Proteins
  • Nuclear Proteins
  • Protein Isoforms
  • TP73 protein, human
  • Tumor Protein p73
  • Tumor Suppressor Proteins