Oncogenic potential of a dominant negative mutant of interferon regulatory factor 3

摘要: Interferon regulatory factor 3 (IRF3) is activated in response to various environmental stresses including viral infection and DNA-damaging agents. However, the biological function of IRF3 cell growth not well understood. We demonstrated that markedly inhibited colony formation cells. blocked DNA synthesis induced apoptosis. Based on this negative control by IRF3, we examined whether functional loss may contribute oncogenic transformation. activity was specifically expression its dominant mutant. This mutant lacks a portion binding domain like IRF3a, an alternative splice form inhibition specific target genes. Mutant efficiently transformed NIH3T3 cells, as anchorage-independent soft agar tumorigenicity nude mice. These results imply tumor suppressor suggest possible role for relative levels tumorigenesis.