Mutant p53 drives cancer by subverting multiple tumor suppression pathways

Sue Haupt, Dinesh Raghu, Ygal Haupt

Research output: Contribution to journalArticleResearchpeer-review

52 Citations (Scopus)

Abstract

The tumor suppressor p53 normally acts as a brake to halt damaged cells from perpetrating their genetic errors into future generations. If p53 is disrupted by mutation, it may not only lose these corrective powers, but counterproductively acquire new capacities that drive cancer. A newly emerging manner in which mutant p53 executes its cancer promoting functions is by harnessing key proteins, which normally partner with its wild type, tumor-inhibiting counterpart. In association with the subverted activities of these protein partners, mutant p53 is empowered to act across multiple fundamental cellular pathways (regulating cell division and metabolism) and corrupt them to become cancer promoting.
Original languageEnglish
Article number12
Number of pages7
JournalFrontiers in Oncology
Volume6
DOIs
Publication statusPublished - 27 Jan 2016

Keywords

  • p53 mutations
  • gain of function
  • metabolism
  • cell cycle
  • transcriptional regulation

Cite this