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Central role of interferon regulatory factor‐1 (IRF‐1) in controlling retinoic acid inducible gene‐I (RIG‐I) expression

Retinoic acid inducible gene‐I (RIG‐I) functions as the first line of defense against viral infection by sensing dsRNA and inducing type I interferon (IFN) production. The expression of RIG‐I itself is induced by IFN‐α/β and dsRNA. To comprehend the molecular mechanism of expression regulation, we cloned the RIG‐I promoter and analyzed its activity upon IFN‐β and dsRNA treatment. Under basal condition, RIG‐I mRNA level and promoter activity were significantly higher in normal cells versus their tumor counterparts. In both normal and cancer cells, RIG‐I expression was induced by IFN‐β and dsRNA. A single IRF‐1 binding site in the proximal promoter functioned as a crucial regulator of basal, IFN‐β‐ and dsRNA‐mediated induction of the RIG‐I promoter. IFN‐β and dsRNA treatment increased IRF‐1 binding to the RIG‐I promoter. IRF‐1 expression was also higher in normal cells than in cancer cells and it was induced by IFN‐β with similar kinetics as RIG‐I. These results confirm that by controlling RIG‐I expression, IRF‐1 plays an essential role in anti‐viral immunity. IRF‐1 is a tumor suppressor and the expression profile of RIG‐I together with its regulation by IRF‐1 and the presence of a caspase‐recruitment domain in RIG‐I suggest that RIG‐I might also possess tumor suppressor properties. J. Cell. Physiol. 213: 502–510, 2007. © 2007 Wiley‐Liss, Inc.