表观遗传学介导肿瘤生物学特性持续被关注，rRNA甲基化作为新型表观遗传方式主要通过NOP58与snoRNA形成复合体介导肿瘤发生发展。课题组分析大肠癌组织LncRNA-snoRNA-mRNA芯片发现ZFAS1、SNORD12家族及NOP58均异常高表达，同步检测到rRNA 2’-O-甲基化显著上升，表明大肠癌存在SNORD12家族调控rRNA甲基化；进一步发现并验证ZFAS1与NOP58存在特异结合。那么ZFAS1是否通过结合NOP58募集SNORD12家族调控rRNA甲基化进而介导大肠癌生物学特性？本项目拟：①明确SNORD12家族介导rRNA甲基化与ZFAS1募集NOP58的相关性；②确认NOP58与ZFAS1关键结合序列；③解析NOP58被ZFAS1特异结合介导rRNA甲基化修饰。本项目旨在研究rRNA甲基化介导大肠癌生物学特性的新机制，为挖掘大肠癌表观遗传调控修饰新靶点提供新思路。

Tumor biological characteristics mediated by epigenetic modification continues to be concerned. rRNA methylation as a new epigenetic method mainly mediates the development of tumor through the formation of NOP58 and snoRNA complex. We analyzed the LncRNA-snoRNA-mRNA tissues array of colorectal cancer, and found that ZFAS1, SNORD12 family and NOP58 were all specifically up-regulated and rRNA 2 '-O- methylation significantly increased, indicating that SNORD12 family regulates rRNA methylation in colorectal cancer. We further identified and verified that there were the specific binding sites between ZFAS1 and NOP58. Can ZFAS1 directly bind to NOP58, and then regulate the characteristics of CRCs through SNORD12 family mediated ribosome RNA 2’-O-methylation? Therefore, this project proposed to ① validate the correlation between SNORD12 family mediated rRNA methylation and ZFAS1 recruitment of NOP58; ② confirm the key binding sequences and sites of NOP58 and ZFAS1; ③ analyze the rRNA methylation modification mediated by ZFAS1 specific binding of NOP58. The aim of this project is to study the new mechanism of rRNA methylation mediating the biological characteristics of colorectal cancer, and provide a new idea for exploring new targets modified by epigenetic regulation of colorectal cancer.