FAM64A positively regulates STAT3 activity to promote Th17 differentiation and colitis-associated carcinogenesis.

is a transcription factor that plays central roles in various physiological processes, including differentiation of Th cells. Its deregulation results in serious diseases, including inflammatory diseases and cancer. The mechanisms related to how duanyu18133 activity is regulated remain enigmatic. Here we show that overexpression of FAM64A potentiates IL-6-induced activation of duanyu18133 and expression of downstream target genes, whereas deficiency of FAM64A has the opposite effects. FAM64A interacts with duanyu18133 in the nucleus and regulates binding of duanyu18133 to the promoters of its target genes. Deficiency of Fam64a significantly impairs differentiation of Th17 but not Th1 or induced regulatory T cells (iTreg). In addition, Fam64a deficiency attenuates experimental autoimmune encephalomyelitis (EAE) and dextran sulfate sodium (DSS)-induced colitis, which is correlated with decreased differentiation of Th17 cells and production of proinflammatory cytokines. Furthermore, Fam64a deficiency suppresses azoxymethane (AOM)/DSS-induced colitis-associated cancer (CAC) in mice. These findings suggest that FAM64A regulates Th17 differentiation and colitis and inflammation-associated cancer by modulating transcriptional activity of

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