The p53-estrogen Receptor Loop in Cancer

Curr Mol Med. 2013 Sep;13(8):1229-40. doi: 10.2174/15665240113139990065.

Abstract

Tumor suppressor p53 maintains genome stability by regulating diverse cellular functions including cell cycle arrest, apoptosis, senescence and metabolic homeostasis. Mutations in the p53 gene occur in almost all human cancers with a frequency of up to 80%. However, it is only 20% in breast cancers, 18% in endometrial cancers and 1.5% in cervical cancers. Estrogen receptor alpha (ERα) plays a pivotal role in hormone-dependent cancer development and the status of ERα is used for designing treatment strategy and for prognosis. A closer look at the cross-talk between p53 and ERα has revealed that their activities are mutually regulated. This review will summarize the current body of knowledge on p53, ERα and ERβ in cancer. Clinical correlations between estrogen receptors and p53 status have also been reported. Thus, this review will discuss the relationship between p53 and ERs at both the molecular and clinical levels.

Publication types

  • Review

MeSH terms

  • Animals
  • Estrogens / metabolism
  • Estrogens / pharmacology
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Neoplasms / genetics
  • Neoplasms / metabolism*
  • Receptors, Estrogen / genetics
  • Receptors, Estrogen / metabolism*
  • Signal Transduction*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Estrogens
  • Receptors, Estrogen
  • Tumor Suppressor Protein p53