前列腺癌发病及转移的机制繁多但不明确。我们前期研究发现：肥胖相关基因FTO表达水平随前列腺癌恶性程度增高而下调，细胞水平功能实验显示FTO发挥抑癌基因作用，同时FTO的启动子区域CpG岛甲基化修饰显著增加，进一步对DNA甲基化修饰酶DNMT1酶RIP-seq，结果鉴定到一条新的lncRNA FTO-MRT。据此提出科学假说：FTO-MRT招募DNA甲基化酶DNMT1到FTO的启动子区域，将胞嘧啶位点修饰为甲基化胞嘧啶，通过抑制FTO转录下调FTO表达水平，增强前列腺癌细胞的增殖和运动能力，发挥促癌lncRNA的功能。本项目拟从lncRNA调控FTO甲基化着手，在细胞、动物和临床三个水平，通过GOF/LOF等手段探索FTO-MRT的体内、体外功能，并结合生物信息学预测、CLIP等实验揭示FTO-MRT的结合调控方式以及对FTO转录的作用机制，为前列腺癌的精准治疗提供新的靶点和理论基础。

Prostate cancer pathogenesis is regulated by numerous unclear factors. Based on previous research of the FTO gene function, methylation modification of its promoter cytosine mediated by DNMT1 binding lncRNA FTO-MRT, we propose the hypothesis that lncRNA FTO-MRT exert its function of regulating methylation transformation via direct recruiting DNMT1which results in the methylated cytosine in FTO gene promoter CpG island and its depressed expression. The attenuated expression of FTO promotes cells proliferation and migration and induces prostate cancer metastasis .In the following study, we intend to explore the function of FTO-MRT in the process of FTO gene promoter CpG island methylation, the related mechanism how FTO-MRT recruits DNMT1 and evaluate the role of FTO-MRT as a biomarker for the diagnosis and prognosis of prostate cancer. The research would provide the evidence of FTO-MRT as a potential target and the basis for the precision therapy of prostate cancer.