组蛋白乙酰化是组蛋白翻译后修饰的一种的重要方式，在调控真核生物的基因表达中发挥着至关重要的作用。组蛋白乙酰化可参与多种细胞生物过程，因此，其异常调控与人类的多种疾病发生相关。这一修饰方式由组蛋白乙酰转移酶(HATs)和组蛋白去乙酰转移酶(HDACs)共同调节。MOF，也称MYST1或KAT8，是组蛋白乙酰转移酶MYST家族(Moz-Ybf2／Sas3-Sas2-Tip60)的一员。 MOF存在于两种蛋白复合物(MSL和NSL)中发挥其生物学功能。这两种复合物均可催化组蛋白H4第16位赖氨酸(H4K16)的乙酰化，而NSL复合物还可乙酰化H4K5和H4K8位点。 MOF可调控多种细胞过程，在基因转录活性调控、维持基因组稳定性、DNA损伤修复、细胞周期调控及早期胚胎发育中发挥着重要作用。MOF及其相关复合物活性异常可引起严重的细胞功能障碍，从而导致细胞死亡或细胞恶性增殖。研究证明，MOF及其作用底物H4K16的乙酰化水平缺失已成为人类肿瘤的一个普遍标志。但也有研究发现MOF在非小细胞肺癌组织中高表达，可见MOF在肿瘤发生中的调控作用是复杂多样的，这提示我们MOF在不同肿瘤中的可能存在不同的调控靶点。 MOF除了在肿瘤疾病中发挥重要作用外，有研究报道MOF可调控T细胞的分化，T细胞特异性敲除MOF可导致小鼠免疫功能丧失，这表明MOF在调控T细胞功能中的重要性。另有研究报道在炎症性肠病患者的结肠组织中H4K16的乙酰化水平存在异常，提示MOF可能在炎症性疾病中同样发挥重要作用。 本研究分为两个部分，第一部分初步探讨了MOF在实验性结肠炎小鼠炎症发生中的作用及可能的调控机制，第二部分研究了MOF对乳腺癌中雌激素受体ERα表达的调控作用及机制，本研究的发现及得出的结论将丰富我们对MOF调控炎症疾病及乳腺癌肿瘤作用机制的理解，并可能成为一个新的治疗靶点。

 Histone acetylation is an important way of histone post-translational modification and plays an important role in the regulation of gene expression in eukaryotes. Histone acetylation can participate in a majority of cell biology processing. Therefore, the abnormal regulation of histone acetylation modification is associated with the occurrence of many kinds of disease. This modification is regulated by histone acetyltransferase (HATs) and deacetyltransferase (HDACs). MOF, also known as MYST1 or KST8, is a member of the of histone acetyltransferase MYST family (moz-ybf2 / sas3-sas2-tip60). MOF performs biological functions in human cells with two different protein complexes (MSL and NSL). Both complexess can catalyze the acetylation of H4K16, however, the NSL complex can also acetylate histone H4K5 and H4K8. MOF can participate in the regulation of various cell processes and plays an important role in gene transcriptional regulation, DNA damage repair , maintaining genomic stability, cell cycle regulation and early embryo development. Abnormal activity of MOF can cause serious cell dysfunction, leading to cell death or uncontrolled cell proliferation. Studies have shown that the absence of MOF and H4K16ac has become a common marker of human tumors. But some studies have found that MOF increased in non-small cell lung cancer tissue. It suggests that the role of MOF in tumorigenesis is complicated. This imply the importance of looking for the MOF specific regulation targets in different cancer. In addition to playing an important role in tumor diseases, some studies have reported that MOF can regulate the differentiation of T cells, and T-cell specific knockout of MOF can lead to the loss of immune function in mice. This indicates the importance of MOF in regulating T cell function. Other studies have reported that abnormal acetylation levels of H4K16 was found in colon tissues of patients with inflammatory bowel disease, suggesting that MOF may play an important role in the regulation of inflammatory diseases. This study is divided into two parts. In the first part, the role and the possible regulatory mechanism of MOF in experimental colitis were preliminarily discussed. The second part studied the role and mechanism of MOF on the expression of estrogen receptor ERα in breast cancer. The findings and conclusions of this study will enrich our understanding of the mechanisms by which MOF regulates inflammatory diseases and breast cancer tumors. This may be a new therapeutic target.