卵巢高级别浆液性癌（HGSOC）隐匿性转移和缺乏靶向治疗是预后差的主要原因。本课题组在“MAP3K3通过持续激活NF-κB通路促进卵巢癌侵袭转移”的前期研究基础上，经预实验发现：LncRNA CTBP1-DT 可能被ETV5 介导转录，竞争性结合miR-188-5p/212-3p，阻断miRs 与MAP3K3的结合，对抗其对MAP3K3 的降解作用，使MAP3K3持续激活并促进HGSOC侵袭转移，但CTBP1-DT的生物学功能和具体作用机制不清。本课题拟1、分析CTBP1-DT—miR-188-5p/212-3p—MAP3K3表达相关性，及CTBP1-DT的预后判断价值；2、阐明CTBP1-DT—miR-188-5p/212-3p—MAP3K3信号轴的调控作用和机制，及对HGSOC生物学行为的影响；3、验证ETV5对CTBP1-DT的转录调控。以期为HGSOC预后判断及治疗提供新靶标。

Early invasion and metastasis, lack of targeted therapy in high-grade serous ovarian cancer (HGSOC) are the major causes of its treatment failure. Based on the results of our previous study, “MAP3K3 promotes ovarian cancer invasion and metastasis by continuously activating NF-κB pathway”, our preliminary experimental date demonstrated that: LncRNA CTBP1-DT and MAP3K3 were consistently expressed in HGSOC cell lines, and both could binding to miR-188-5p/212-3p, which could negatively regulating expression of MAP3K3, expression of CTBP1-DT and MAP3K3 were up-regulated after inhibition of miR-188-5p/212-3p, ETV5 may directly regulating transcription of CTBP1-DT. Those date may suggest that CTBP1-DT may be involved in the regulation of MAP3K3 expression, but its specific function and mechanism is unclear. Therefore, this project will focus on 1. Analyze the correlation between CTBP1-DT-miR-188-5p/212-3p-MAP3K3 expression and prognostic value of CTBP1-DT though scanning of HGSOC tissue samples; 2. Verify the role and regulation mechanism of CTBP1-DT-miR-188-5p/212-3p-MAP3K3 signal axis in the cell and nude mouse model of HGSOC; 3. Certify the transcriptional regulation of ETV5 on CTBP1-DT.