Clinical Significance
In myeloid cells, IRF8 regulates the expression of Bax and Fas to regulate apoptosis. In chronic myelogenous leukemia (CML), IRF8 regulates acid ceramidase to mediiate CML apoptosis.
IRF8 is highly expressed in myeloid cells and was originally identified in as a critical linage-specific transcription factor for myeloid cell differentiation, recent studies, however, have shown that IRF8 is also constitutively expressed in non-hematopoietic cancer cells, albeit at a lower level. Furthermore, IRF8 can also be up-regulated by IFN-γ in non-hemotopoietic cells. IRF8 mediates the expression of Fas, Bax, FLIP, Jak1 and STAT1 to mediate apoptosis in non-hemotopoietic cancer cells.
Analysis of human cancer genomics database revealed that IRF8 is not significantly focally amplified across the entire dataset of 3131 tumors, but is significantly focally deleted across the entire dataset of 3131 tumors, suggesting that IRF8 is potentially a tumor suppressor in humans. Molecular analysis indicated that the IRF8 gene promoter is hypermethylated in human colon carcinoma cells, suggesting that these cells might use DNA methylation to silence IRF8 expression to advance the disease.
Read more about this topic: Interferon Consensus Sequence-binding Protein
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