Requirement of NF-κB Activation to Suppress p53-Independent Apoptosis Induced by Oncogenic Ras
摘要：
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-κB). 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-κB. These results provide an explanation for the requirement of NF-κB 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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关键词：
Animals Mice Rats 3T3 Cells Cell Transformation, Neoplastic NF-kappa B Adenovirus E1A Proteins Transfection Genes, p53 Genes, ras
DOI：
10.1126/science.278.5344.1812
被引量：
年份：
1997
Semantic Scholar
掌桥科研
万方医学
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