淋巴转移是影响宫颈癌复发与预后的重要因素。淋巴管新生是宫颈癌淋巴转移的关键步骤，其调控机制目前尚不清楚。研究表明淋巴内皮细胞(LECs)糖酵解异常参与调控淋巴管新生，外泌体介导的信号传递与糖酵解存在密切联系。前期研究证实miR-206/c-Met在LECs糖酵解调控中发挥重要作用，进一步发现宫颈癌细胞来源外泌体UCA1可增强LECs内c-Met表达并促进淋巴脉管形成。本课题拟从糖酵解的角度入手，通过临床标本、细胞和动物等多层面探究宫颈癌来源外泌体UCA1对淋巴管新生的调控作用，解析外泌体UCA1对LECs内miRNA及mRNA表达谱的影响，明确UCA1与c-Met竞争性结合miR-206在增强LECs糖酵解进而促淋巴管新生的作用机制。本项目旨在探讨外泌体UCA1/miR-206/c-Met信号途径在宫颈癌淋巴管新生中的作用，通过甄别该信号途径中的关键靶点为宫颈癌淋巴转移提供新的阻断策略。

Lymphatic metastasis is an important factor affecting the recurrence and prognosis of cervical cancer. Lymphangiogenesis is a key step in lymphatic metastasis of cervical cancer, and its regulatory mechanism is still unclear. Studies have shown that abnormal glycolysis of lymphatic endothelial cells (LECs) is involved in the regulation of lymphatic angiogenesis, and exosome-mediated signal transduction is closely related to glycolysis. Previous studies have confirmed that miR-206/c-Met played a crucial role in the regulation of glycolysis of lymphatic endothelial cells. It was further found that cervical cancer cell-derived exosomal UCA1 could enhance the expression of c-Met in lymphatic endothelial cells and promote lymphatic angiogenesis. From the perspective of glycolysis, this research aims to explore the regulatory effect of UCA1 on lymphangiogenesis by clinical specimens, cell and animal models, to analyze the influence of UCA1 on the expression profile of microRNAs and mRNAs in lymphoendothelial cells, and to clarify the role of competitive binding of UCA1 and c-Met to miR-206 in promoting the lymphangiogenesis by enhancing the glycolysis of lymphatic endothelial cells. The purpose of this project is to investigate the role of exosome UCA1/miR-206/c-Met signaling pathway in lymphangiogenesis of cervical cancer, and to provide a new strategy for blocking lymphatic metastasis of cervical cancer by identifying key targets in this signaling pathway.