Requirement of NF-κB activation to suppress p53-independent apoptosis induced by oncogenic ras

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  • Mayo, Marty W.
    • Affiliation: N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center
  • Wang, Cun-Yu
    • Affiliation: N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center
  • Cogswell, Patricia C.
    • Affiliation: N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center
  • Rogers-Graham, Kelley S.
    • Affiliation: School of Medicine, Department of Pharmacology
  • Lowe, Scott W.
    • Other Affiliation: Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
  • Der, Channing
    • Affiliation: N.C. Cancer Hospital, UNC Lineberger Comprehensive Cancer Center
  • Baldwin, Albert
Abstract
  • The ras proto-oncogene is frequently mutated in human tumors and functions to chronically stimulate signal transduction cascades resulting in the synthesis or activation of specific transcription factors, including Ets, c-Myc, c-Jun, and nuclear factor kappa B (NF-kappaB). These Ras-responsive transcription factors are required for transformation, but the mechanisms by which these proteins facilitate oncogenesis have not been fully established. Oncogenic Ras was shown to initiate a p53-independent apoptotic response that was suppressed through the activation of NF-kappaB. These results provide an explanation for the requirement of NF-kappaB for Ras-mediated oncogenesis and provide evidence that Ras-transformed cells are susceptible to apoptosis even if they do not express the p53 tumor-suppressor gene product.
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  • Journal Item
Rights statement
  • In Copyright
Journal title
  • Science
Journal volume
  • 278
Journal issue
  • 5344
Page start
  • 1812
Page end
  • 1815
Language
  • English
Version
  • Postprint
ISSN
  • 0036-8075

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