MYC and the control of apoptosis

Cold Spring Harb Perspect Med. 2014 Jul 1;4(7):a014407. doi: 10.1101/cshperspect.a014407.

Abstract

MYC expression is tightly correlated with cell-cycle progression in normal tissues, whereas unchecked MYC expression is among the most prominent hallmarks of the hyperproliferation associated with most forms of cancer. At first glance it might seem counterintuitive that MYC is also among the most robust agents of programmed cell death (apoptosis) in mammalian cells. However it is clearly beneficial for a multicellular organism to have a mechanism for triggering death in cells that express potentially oncogenic levels of MYC. Decades of intense study have begun to provide an understanding of the mechanisms that regulate MYC's seemingly split personality. Key features of MYC-induced apoptosis will be discussed here along with examples of how our understanding of this pathway might be exploited for the therapeutic benefit of cancer patients.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Disease Models, Animal
  • Genes, myc / physiology*
  • Humans
  • Mice
  • Neoplasms / genetics*
  • Neoplasms / therapy
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / physiology
  • Proto-Oncogene Proteins c-myc / physiology*
  • Tumor Suppressor Protein p53 / physiology

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-myc
  • Tumor Suppressor Protein p53