Apoptotic cell death induced by c-myc is inhibited by bcl-2

Nature. 1992 Oct 8;359(6395):552-4. doi: 10.1038/359552a0.

Abstract

Apoptosis is a form of physiological cell death, characterized by chromatin condensation, cytoplasmic blebbing and DNA fragmentation, which often depends on RNA and protein synthesis by the dying cell. The c-myc proto-oncogene, usually implicated in cell transformation, differentiation and cell-cycle progression also has a central role in some forms of apoptosis. These opposing roles of myc in cell growth and death require that other gene products dictate the outcome of c-Myc expression on a cell. A candidate for such a modifying gene is bcl-2, whose product prolongs cell survival and blocks apoptosis in some systems. Here we demonstrate that Bcl-2 prevents apoptotic death induced by c-Myc, provide a mechanism whereby cells can express c-Myc without undergoing apoptosis, and give a possible explanation for the ability of Bcl-2 to synergize with c-Myc in cell transformation.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Blotting, Western
  • CHO Cells
  • Cell Death / genetics*
  • Cricetinae
  • Gene Expression
  • Genes, myc / physiology*
  • Hot Temperature
  • Kinetics
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins c-bcl-2
  • Transfection

Substances

  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2