宫颈癌是女性生殖系统最常见恶性肿瘤。早期宫颈癌中盆腔淋巴结转移的发生率高达27%，严重影响患者预后。宫颈癌淋巴结转移的具体调控机制目前仍不明确，极大制约了宫颈癌治疗方案个体化进展。前期研究首次发现HPV16 E7可能通过增加癌旁组织淋巴管密度促进宫颈癌淋巴结转移，且利用蛋白质谱芯片技术发现HPV16 E7与HMGA1以相互作用蛋白的形式参与宫颈癌淋巴结转移。本项目拟在前期研究的基础上，利用CHIP-seq、细胞因子芯片、荧光素酶报告系统、CRISPR/Cas9、动物活体成像等技术明确HPV16 E7-HMGA1-淋巴管生成在宫颈癌淋巴结转移中的作用模式，进而深入研究发挥效应的下游信号通路并靶向干预关键分子。旨在全面揭示HPV16 E7介导宫颈癌淋巴结转移的具体调控机制，从而为临床上辅助制定个体化治疗、改善预后提供理论依据。

Cervical cancer is the most common cancer of the female reproductive system. 27% patients accompanied with lymph node metastasis in early cervical cancer, presented poor prognosis. The exact mechanism of cervical cancer metastasis by lymphatic vessel is still unclear, which severely restricts individual therapy progression. Our preliminary experiments demonstrated that HPV16 E7 coud induce cervical cancer metastasis and correlate with density of lymphatic vessels in paratumor, in which HMGA1 might play a particular role, but the specific regulating mechanism is still uncertain. Therefore, based on the in vitro and vivo model, CHIP-seq, microarray, Luciferase reporter system, CRISPR/Cas9 technique, we plan to identify the mechanism of HPV16 E7-HMGA1-lymphangiogenesis in cervical cancer lymphatic metastasis, furthermore, investigate the detailed signal pathways and the key molecules involved in HPV16 E7-mediated lymphangiogenesis. The purpose was to clarify the mechanism of HPV16 E7 induced lymphangiogenesis in cervical cancer, develop idea for cervical cancer lymphatic metastasis, provide molecular evidence for clinical individual treatment and improving prognosis.