| Literature DB >> 8062214 |
N Tanaka1, M Ishihara, T Taniguchi.
Abstract
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.Entities:
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Year: 1994 PMID: 8062214 DOI: 10.1016/0304-3835(94)90318-2
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679