人类特有lncRNA：CDK1AR在胶质瘤发生发展中的功能及机制研究

胶质瘤是发病率最高的脑恶性肿瘤，因其增殖能力强、迁移速度快、复发率高特点，胶质瘤的治疗一直困扰着临床一线医生。近年来，由于基因测序技术和RNA研究的高速发展，过去被认为几无作用的非编码RNA逐渐显露头角。课题组通过对胶质瘤标本进行转录组测序和生信分析发现，CDK1AR的表达上调与胶质瘤的不良预后密切相关；前期工作表明敲低CDK1AR可显著抑制胶质瘤的增殖、迁移并促进细胞的凋亡；机制实验显示敲低CDK1AR可通过抑制p21/p27通路并抑制周期蛋白CDK1磷酸化进而影响细胞周期。本项目拟在前期工作的基础上，通过增加临床实验样本数据和细胞实验，进一步发掘CDK1AR与胶质瘤恶性表型的相关关系和更为详尽的机制通路，并通过动物体内实验对前期结果进行验证，以期发现胶质瘤治疗的新靶点并为胶质瘤的基础研究和临床治疗提供新的实验室基础。

Glioma has the highest incidence within brain malignant tumor. Because of its proliferation ability, migration speed and high recurrence rate, the treatment of glioma has always troubled clinical doctors. In recent years, due to the rapid development of gene sequencing technology and RNA research, non-coding RNA that used to be considered inadequate has gradually emerged. Our team conducted transcriptome sequencing and bio-information analysis on glioma specimens and found that the up-regulation of CDK1AR is closely related to the poor prognosis of glioma; previous work has shown that CDK1AR can significantly inhibit the proliferation and migration of glioma and further cells Mechanism experiments show that CDK1AR can affect the cell cycle by inhibiting the p21/p27 pathway and inhibiting the phosphorylation of CDK1. Based on the preliminary work, this project intends to further explore the correlation between CDK1AR and the malignant phenotype of glioma and more detailed mechanism pathways through increasing clinical erimental sample data and cell experiments, and conduct in vitro experimental results through animal experiments to verify previous trials, with a view to discovering new targets for glioma treatment and providing a new laboratory basis for basic research and clinical treatment of glioma.