Apoptotic cell death induced by c-myc is inhibited by bcl-2.
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.
Bissonnette
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Division of Cellular Immunology, La Jolla Institute for Allergy and Immunology, California 92037.
Echeverri
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F
Mahboubi
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A
Green
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DR
D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D015153:Blotting, Western; D016466:CHO Cells; D016923:Cell Death / Q000235:genetics*; D006224:Cricetinae; D015870:Gene Expression; D016259:Genes, myc / Q000502:physiology*; D006358:Hot Temperature; D007700:Kinetics; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D019253:Proto-Oncogene Proteins c-bcl-2; D014162:Transfection
D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2