lncRNA-SNHG1核质转换及对p53双向调控在结肠癌中的功能与机制

结肠癌是常见的消化道恶性肿瘤，在我国发病率呈现逐年增高的趋势。我们前期发现抗癌药物阿霉素在结肠癌细胞中可诱导lncRNA SNHG1发生核质定位转换，而且SNHG1在胞质及胞核中对p53具有完全相反的双向调控作用，分别发挥癌基因及抑癌基因的功能。在上述研究基础上，本项目的拟通过系列研究阐明lncRNA SNHG1在结肠癌发生发展过程中核质定位规律，揭示lncRNA SNHG1在细胞质与细胞核中对p53的双向调控作用和分子机制，以及阿霉素等抗癌药物作用时SNHG1定位转换的分子机理。本项目将从lncRNA核质定位转换这一新的角度，为结肠癌的诊断和药物治疗提供新的理论方法支持。

Colorectal cancer is a common malignant tumor of the digestive tract, the incidence rate increased year by year in China. In our preliminary experiment, we found that anticancer drug doxorubicin can induce nucleus-cytoplasm translocation of lncRNA SNHG1 in colon cancer cells. SNHG1 can regulate p53 expression in opposite direction in cell nucleus and cytoplasm, respectively, and play opposite roles in colon cancer cells. Based on the above research, the aim of this project is to elucidate the localization rule of lncRNA SNHG1 in the development and progression of colorectal cancer, reveal the bi-directional regulation and molecular mechanism of lncRNA SNHG1 in cytoplasm and nucleus, and the molecular mechanism of SNHG1 nucleus-cytoplasm translocation induced by doxorubicin. This will provide novel theory and method for colorectal cancer diagnosis and drug treatment by lncRNA nucleus-cytoplasm translocation.