| Literature DB >> 8004672 |
N Tanaka1, M Ishihara, M Kitagawa, H Harada, T Kimura, T Matsuyama, M S Lamphier, S Aizawa, T W Mak, T Taniguchi.
Abstract
The transcriptional activator interferon regulatory factor 1 (IRF-1) and its antagonistic repressor IRF-2 are regulators of the interferon (IFN) system and of cell growth. Here we report that embryonic fibroblasts (EFs) from mice with a null mutation in the IRF-1 gene (IRF-1-/- mice) can be transformed by expression of an activated c-Ha-ras oncogene. This property is not observed in EFs from wild-type or IRF-2-/- mice but is still observed in EFs from mice deficient in both genes. The transformed phenotype of ras-expressing IRF-1-/- EFs could be suppressed by the expression of the IRF-1 cDNA. Thus, IRF-1 functions as a tumor suppressor. Furthermore, expression of the c-Ha-ras oncogene causes wild-type but not IRF-1-/- EFs to undergo apoptosis when combined with a block to cell proliferation or treated by anticancer drugs or ionizing radiation. Hence, IRF-1 may be a critical determinant of oncogene-induced cell transformation or apoptosis.Entities:
Mesh：
Substances：
Year: 1994 PMID： 8004672 DOI： 10.1016/0092-8674(94)90132-5
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582