淋巴结转移是早期宫颈癌致死的主要原因。研究表明脂肪酸代谢重塑可促进多种恶性肿瘤发生淋巴结转移。我们前期工作证实脂肪酸代谢中枢调控分子脂肪酸结合蛋白5（FABP5）可促进宫颈癌淋巴结转移；预实验发现干扰lncRNA RP11-363E6.3可抑制FABP5，导致脂肪酸代谢关键酶表达失常，使得宫颈癌细胞侵袭迁移能力显著降低。由此我们假设：lncRNA RP11-363E6.3可调控FABP5介导的脂肪酸代谢重塑，从而促进宫颈癌淋巴结转移。为此，本项目拟进一步明确FABP5介导的脂肪酸代谢重塑在lncRNA RP11-363E6.3促进宫颈癌淋巴结转移中的作用；阐明lncRNA RP11-363E6.3通过脂肪酸代谢重塑激活EMT及PPARδ/VEGF通路的调控机制。本研究从lncRNA调控脂肪酸代谢重塑的角度揭示宫颈癌淋巴结转移的新机制，为实现宫颈癌个体化精准治疗，提高患者整体预后提供新策略。

Lymph node metastasis is the major cause of death in early-stage cervical cancer. Studies have shown that the reprogramming of fatty acid metabolism can promote metastasis of lymph node in a variety of malignant tumors. In our previous work, fatty acid binding protein 5 (FABP5) which a central regulatory molecule of fatty acid metabolism ,can promote lymph node metastasis of cervical cancer. Preliminary experiments found that knockdown of lncRNA RP11-363E6.3 suppressed FABP5, resulted in aberrant expression of key enzymes of fatty acid metabolism and significantly reduced metastatic ability of cervical cancer cells. Thus we assume that lncRNA RP11-363E6.3 regulates FABP5-mediated reprogramming of fatty acid metabolism to promote lymph node metastasis in cervical cancer. Therefor, this project intends to further clarify the role of FABP5-mediated reprogramming of fatty acid metabolism in lymph node metastasis promoted by lncRNA RP11-363E6.3; to establish the mechanism of lncRNA RP11-363E6.3 activating EMT and PPARδ/VEGF through reprogramming of fatty acid metabolism. This study reveal new mechanisms of lymph node metastasis from the perspective of fatty acid metabolism reprogromming mediated by lncRNA, and provide a new strategy for achieving individualized precision treatment of cervical cancer as well as improving its overall prognosis.