In Perspective
The paradox of E2F1: Oncogene and tumor suppressor gene
David G. Johnson,
Corresponding Author
David G. Johnson
Department of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science Park–Research Division, Smithville, Texas
Department of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science Park–Research Division, P. O. Box 389, Smithville, TX 78957.Search for more papers by this authorDavid G. Johnson,
Corresponding Author
David G. Johnson
Department of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science Park–Research Division, Smithville, Texas
Department of Carcinogenesis, The University of Texas M. D. Anderson Cancer Center, Science Park–Research Division, P. O. Box 389, Smithville, TX 78957.Search for more papers by this authorFirst published: 07 March 2000
Citations: 79
Abstract
Cancer cells often contain mutations that lead to the loss of retinoblastoma tumor suppressor (Rb) function and the activation of E2F-dependent transcription. As a result, proliferation is deregulated, and sensitivity to apoptotic stimuli is increased. In cell culture studies, the transcription factor E2F1 has been shown to be equally adept at inducing proliferation and apoptosis. Several groups using mouse models have been examining how these E2F1-regulated processes impact the development of cancer. The conclusion from these studies is that E2F1 can function as both oncogene and tumor suppressor gene and that both positive and negative effects on tumorigenesis can be observed whether E2F1 is absent or overexpressed. These findings are discussed in the context of a model in which pathways controlling cell-cycle progression and apoptosis are intimately linked. Mol. Carcinog. 27:151–157, 2000. © 2000 Wiley-Liss, Inc.
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