Transcriptional inhibitors, p53 and apoptoss

Biochim Biophys Acta. 2008 Dec;1786(2):83-6. doi: 10.1016/j.bbcan.2008.04.004. Epub 2008 May 8.

Abstract

Transcriptional inhibitors (TI) repress global transcription and induce apoptosis. It has been suggested that induction of p53 is one of the hallmarks of global transcriptional repression. Two recent papers suggested that treatment of human cancer cells with TIs, leads to p53-dependent, transcription-independent or p53-dependent, transcription-dependent apoptosis. The latter mechanism is linked to the fact that TIs can be selective in their inhibitory effects thereby permitting transcription of some genes. However, the majority of other published data suggest that these drugs induce p53-independent apoptosis. In this article I discuss the mechanisms of TI-dependent cell death and the potential role of p53 in this process.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Apoptosis / drug effects*
  • Cyclin-Dependent Kinase Inhibitor Proteins / physiology
  • Humans
  • Models, Biological
  • RNA Polymerase II / metabolism
  • Transcription, Genetic / drug effects*
  • Tumor Suppressor Protein p53 / physiology*

Substances

  • Cyclin-Dependent Kinase Inhibitor Proteins
  • Tumor Suppressor Protein p53
  • RNA Polymerase II