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. 2013 Feb;5(2):417-423.
doi: 10.3892/ol.2012.1051. Epub 2012 Nov 28.

Function and mechanism by which interferon regulatory factor-1 inhibits oncogenesis

Affiliations

Function and mechanism by which interferon regulatory factor-1 inhibits oncogenesis

Fei-Fei Chen et al. Oncol Lett. 2013 Feb.

Abstract

The present review focuses on recent advances in the understanding of the molecular mechnisms by which interferon regulatory factor (IRF)-1 inhibits oncogenesis. IRF-1 is associated with regulation of interferon α and β transcription. In addition, numerous clinical studies have indicated that IRF-1 gene deletion or rearrangement correlates with development of specific forms of human cancer. IRF-1 has been revealed to exhibit marked functional diversity in the regulation of oncogenesis. IRF-1 activates a set of target genes associated with regulation of the cell cycle, apoptosis and the immune response. The role of IRF-1 in the regulation of various types of human tumor has important implications for understanding the susceptibility and progression of cancer. In addition, an improved understanding of the role of IRF-1 in the pathological processes that lead to human malignant diseases may aid development of novel therapeutic strategies.

Keywords: IRF-1; apoptosis; cell cycle; immune response; oncogenesis.

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Figures

Figure 1.
Figure 1.
Structure of IRFs. All IRFs contain an amino-terminal DNA binding domain (DBD) that is characterized by a series of five well-conserved tryptophan-rich repeats (grey) and a regulatory domain (yellow). The DBD forms a helix-turn-helix domain and recognizes a DNA sequence similar to the IFN-stimulated response element. The majority of IRFs also contain an IRF-association domain (IAD) of type 1 (IAD1) or type 2 (IAD2). Specific IRFs contain repression domain(s) (red) and a nuclear-import signal(s) (black). For IRF-1, 3, 5 and 7, the mark of red arrows show that activity depends on phosphorylation. The number of amino acids of each IRF is indicated. IFN, interferon; IRF, IFN regulatory factor.

References

    1. Mamane Y, Heylbroeck C, Genin P, Algarte M, Servant MJ, LePage C, DeLuca C, Kwon H, Lin R, Hiscott J. Interferon regulatory factors: the next generation. Gene. 1999;237:1–14. - PubMed
    1. Taniguchi T, Ogasawara K, Takaoka A, Tanaka N. IRF family of transcription factors as regulators of host defense. Annu Rev Immunol. 2001;19:623–655. - PubMed
    1. Wathelet MG, Lin CH, Parekh BS, Ronco LV, Howley PM, Maniatis T. Virus infection induces the assembly of coordinately activated transcription factors on the IFN-beta enhancer in vivo. Mol Cell. 1998;1:507–518. - PubMed
    1. Meraro D, Hashmueli S, Koren B, Azriel A, Oumard A, Kirchhoff S, Hauser H, Nagulapalli S, Atchison ML, Levi BZ. Protein-protein and DNA-protein interactions affect the activity of lymphoid-specific IFN regulatory factors. J Immunol. 1999;163:6468–6478. - PubMed
    1. Lohoff M, Mak TW. Roles of interferon-regulatory factors in T-helper-cell differentiation. Nat Rev Immunol. 2005;5:125–135. - PubMed

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