Suppression of c-myc or fosB-induced cell transformation by the transcription factor IRF-1.
The transcriptional activator IRF-1 and its antagonistic repressor IRF-2 are regulators of the interferon (IFN) system and of cell growth. Overexpression of IRF-2 leads to transformation of NIH3T3 cells, and the concomitant overexpression of IRF-1 reverts this transformed phenotype. Here we report that c-myc- or fosB-transformed rat embryonic fibroblast cells can be reverted by the introduction of the IRF-1 gene. Thus, the anti-oncogenic function of IRF-1 is not limited to only IRF-2 overexpressing cells, suggesting the broad role of IRF-1 as a tumor suppressor.
Tanaka
N
N
Institute for Molecular and Cellular Biology, Osaka University, Japan.
Ishihara
M
M
Taniguchi
T
T
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D002478:Cells, Cultured; D004268:DNA-Binding Proteins / Q000502:physiology*; D016147:Genes, Tumor Suppressor; D016762:Genes, fos; D016259:Genes, myc; D050856:Interferon Regulatory Factor-1; D010750:Phosphoproteins / Q000502:physiology*; D051381:Rats; D014157:Transcription Factors / Q000502:physiology; D014162:Transfection
D004268:DNA-Binding Proteins; D050856:Interferon Regulatory Factor-1; C494259:Irf1 protein, rat; D010750:Phosphoproteins; D014157:Transcription Factors