Epigenetic regulation and anti-tumor mechanisms of STAT3 in tumor bearing mouse model

骨髓来源的树突状细胞通过STAT3和hdac的表观遗传调控可能增强抗肿瘤作用。在本研究中，我们证明了STAT3-HDAC7轴在荷瘤小鼠模型中具有关键作用并诱导肿瘤消除。STAT3缺失的树突状细胞显示MHCⅱ类、CD80、86、40和IL-12、IL-6、IL-10表达增强。在该模型中，STAT3结合HDAC7启动子，可能调控细胞因子的表达。因此，hdac通过STAT3独特地调节肿瘤生长。hdac的治疗应用有待进一步阐明。

Epigenetic regulation via STAT3 and HDACs in bone marrow derived dendritic cells potentially enhances anti-tumor effect. In this study, we demonstrated the STAT3-HDAC7 axis had a key role and induces tumor elimination in tumor bearing mouse model. The STAT3 deficient dendritic cells revealed enhanced expression of MHC class II, CD80, 86, 40 and IL-12, IL-6, IL-10 expression. In this model, STAT3 bound HDAC7 promoter and probably regulates cytokine expression. Thus, HDACs uniquely regulate tumor growth with STAT3. And the therapeutic application of HDACi should be elucidated in the future.