RNA腺嘌呤甲基化(m6A)调控是RNA表观遗传学重要研究内容，亦是生命科学新的研究热点。m6A作为一种新的RNA代谢调控因子参与肿瘤发生发展过程，但其与膀胱癌的相关性尚未见报道。我们前期研究首次发现人膀胱癌细胞中肿瘤关键信号通路分子--CUB结构域跨膜糖蛋白1（CDCP1）存在m6A修饰调控，且蛋白表达升高，并促进膀胱癌细胞的迁移。但CDCP1在膀胱癌中作用及其m6A调控机制尚未明确。本项目拟进一步阐明膀胱癌中m6A修饰酶、CDCP1表达及其m6A修饰之间的相关性；通过基因功能获得、缺失及拯救实验策略，揭示m6A RNA甲基化修饰酶及其介导CDCP1 m6A修饰在膀胱癌发生发展中的作用和调控机制；进而利用新型的RCas9技术探索靶向CDCP1 m6A修饰对膀胱癌发生发展的影响。本项目不仅为揭示膀胱癌RNA表观遗传学机制提供重要的理论基础，而且为膀胱癌靶向干预提供新的策略。

N6-methyladenosine (m6A) regulation is an important content of RNA epigenetics. It becomes new hotspot in life science. m6A, as a novel regulator for RNA metablism, is invovled in cancer development. However, the relationship betwent m6A and bladder cancer is unclear. In our previous studies, we first found CUB domain-containing protein1 (CDCP1), as a key molecule for cell signaling pathway in cancer, was regulated by m6A modifications, and high expression of CDCP1 in bladder cancer cells enhanced cells migration. However, biological function and mechanism of CDCP1 and its mRNA m6A modification in bladder cancer development have remained obscure. In this project, we will further identify relationship among enzymes for m6A modification, CDCP1 expression and CDCP1 m6A in bladder cancer. Moreover, we will investigate function and molecular mechanism of m6A modification enzymes and CDCP1 m6A in the occurrence and development of bladder cancer by gain-of-function,loss-of-function and rescure strategy. Furthermore, we will explore effects of targeting m6A modification of CDCP1 on bladder cancer development by RCas9 technology. This project will not only lay an important theoretical foundation for revealing molecular mechanism of bladder cancer RNA epigenetics, but provide a novel strategy for targeted intervention of bladder cancer.