LncRNA在慢性炎症及肿瘤发生中起重要作用，但在“炎-癌”转变中机制不明。本课题组发现lncRNA SH3PXD2A-AS1表达量在溃疡性结肠炎“炎-癌”转变中渐升高，起促增殖、抑凋亡作用，且可能通过STAT通路介导溃疡性结肠炎“炎-癌”转变。据此提出假设：在溃疡性结肠炎中，p-STAT3诱导SH3PXD2A-AS1表达，SH3PXD2A-AS1通过募集绑定CoREST及DNMT1抑制下游靶基因SOCS3、p21，进一步激活STAT通路，加重溃疡性结肠炎，促进溃疡性结肠炎“炎-癌”转变。在申请人既往研究lncRNA及溃疡性结肠炎“炎-癌”转变的基础上，采用ChIP、RIP、RNA-pulldown等技术，以SH3PXD2A-AS1为切入点，探索其对STAT通路的调节作用，揭示其调控溃疡性结肠炎“炎-癌”转变的分子机制，为结肠炎相关性结肠癌的预防和诊断提供部分研究基础和理论依据。

LncRNAs play important roles in chronic inflammation and tumorigenesis, but the underlying mechanisms of lncRNAs remain unclear in the inflammatory-to-cancer process. In our previous study, lncRNA SH3PXD2A-AS1 expression was gradually increased in the inflammatory-to-cancer process of ulcerative colitis(UC). High SH3PXD2A-AS1 expression could promote proliferation and inhibit apoptosis by activation of STAT3 signaling in this process. So, we hypothesized that p-STAT3-induced upregulation of SH3PXD2A-AS1 could repress SOCS3 and p21 expressions by binding to CoREST and DNMT1, and further lead to UC ingravescence and accelerate inflammatory-to-cancer process. Based on our study of lncRNAs and the inflammatory-to-cancer process of UC, we will explore the regulatory effect of SH3PXD2A-AS1 on STAT signaling using ChIP, RIP, RNA-pulldown, and etc. All the findings could reveal the underlying regulatory mechanism of SH3PXD2A-AS1 in the inflammatory-to-cancer process and provide more research and theoretical basis for CAC prevention and diagnosis.