DNA双链断裂(DSB)是放射致基因组不稳定的主要原因，同源重组修复（HR）作为真核生物DSB修复的主要方式之一，其调控机制仍然是放射生物学领域的重要科学问题。长链非编码RNA（LncRNA）被证实具有重要生物学功能，其在DNA损伤修复如HR中的作用代表了一个新的方向领域。Lnc-RI是本实验室发现的一种放射诱导表达lncRNA，前期研究证实，敲低lnc-RI在下调HR通路相关分子PLK1表达的同时，引起DSB增加，提示lnc-RI可能参与放射后DSB的HR修复。本项目就此展开深入研究：1）明确lnc-RI通过PLK1对放射致DSB的HR修复的促进作用；2）分析lnc-RI调节PLK1表达影响HR修复的作用机制；3）验证lnc-RI通过PLK1-RAD51信号通路调节HR修复。上述研究将从lncRNA角度对放射致DSB修复机制提出新的理论阐述，加深对细胞基因组稳定性调控机制认识。

DNA double-strand break (DSB) is the main factor, which induces genomic instability after ionizing radiation. As one of the main ways to repair DSB in eukaryote, homologous recombination repair (HR) is still an important scientific issue in the field of radiation biology. Long non-coding RNA (LncRNA) has been shown to play critical roles in many biological processes. Research on lncRNA which involved in DNA damage repair such as HR repair presents a new study field. Lnc-RI is a lncRNA induced by ionizing radiation found in our laboratory. Our studies previously confirmed that knockdown lnc-RI increased DSB in cells and reduced expression of PLK1 which promote HR repair. These results suggest that lnc-RI may play a role in HR repair of DSBs induced by radiation. This project aims the three issues: 1) Whether lnc-RI promote DSBs HR repair through PLK1 after radiation? 2) What is the mechanism by which lnc-RI regulate plk1 expression and promote HR repair? 3) whether lnc-RI regulated DSB HR repair by PLK1-RAD51? The study will present a new theoretical explanation about radiation-induced DSB repair mechanisms from the perspective of lncRNA, and deepen understanding of regulatory mechanisms of cellular genome stablity.