课题组前期研究发现基因组许多位点组蛋白H3R2甲基化不受甲基转移酶PRMT6影响，说明体内存在其它H3R2甲基转移酶； PRDM10含SET结构域，检测发现其可以催化未修饰的组蛋白H3，但无法催化H3R2甲基化的组蛋白，说明PRDM10可能是组蛋白甲基转移酶，催化位点可能是H3R2。PRDM10在多种肿瘤中异常表达，且可能在肿瘤中与PRDM14相互作用；多种肿瘤中发现其酶活结构域突变，可能影响甲基转移酶活性；故推测，PRDM10通过组蛋白甲基转移酶活性以及与PRDM14的相互作用参与肿瘤发生。为证实以上假设，本项目采用体外甲基转移酶酶活实验检测PRDM1O的组蛋白催化活性；基因转染调节乳腺癌细胞PRDM10水平，做功能恢复实验，观察甲基转移酶活性的生物功能；利用ChIP-seq研究PRDM1O的全基因组分布，结合表达谱芯片，串联亲和纯化寻找直接调控的基因并建立蛋白作用网络，为干预有效的信号环节或研发新型抗癌药物奠定基础。

Our previous studies have shown some histone H3 arginine 2(H3R2) methylation in the genome is not affected by PRMT6,means new H3R2 methylases exist;PRDM10 is PR/SET family members,our data show it can methylate unmodified H3,but not H3R2me,so PRDM10 would be Novel histone Methyltransferase ; PRDM10 might play an essential role in tumorigenesis because of its abnormal expression in some tumors;also,Mutations in PRDM10 SET domain occurred in high frequence in several cancers, also it can interact with PRDM14,demonstrate the possible association between histone methytransferase activity and tumorigenesis.in our study, we will confirm the H3 methylation activity of PRDM10 by histone methylation assay;cell transfection will be done to regulate PRDM1O expression in breast cancer cells,and resuce experiment will be designed to see the biological function of PRDM10 histone methlation activity. distribution and gene expression profile of PRDM10 will be detected by ChIP-seq and microarray, Tandem Affinity Purification assay will be used to establish protein interation network.