半乳糖凝集素-3通过Wnt/β-Catenin通路调控上皮性卵巢癌转移及化疗敏感性的研究

广泛种植性转移和化疗耐药是上皮性卵巢癌治疗失败的主要原因，但具体机制却仍不清楚。我们前期研究发现调控半乳糖凝集素-3（Gal-3）能影响卵巢癌细胞的转移能力与化疗敏感性，并引起β-Catenin相应变化，且在组织标本中，Gal-3与β-Catenin表达成正相关，提示Gal-3可能通过Wnt/β-Catenin通路起作用。本研究拟在前期研究的基础上，采用免疫共沉淀、westernblot和免疫荧光等技术，研究Gal-3如何通过Wnt/β-Catenin通路调控上皮性卵巢癌细胞转移能力和对卡铂/紫杉醇的敏感性，构建Gal-3过表达和低表达的上皮性卵巢癌裸鼠模型，验证Gal-3通过Wnt/β-Catenin通路调控其转移能力和对卡铂/紫杉醇敏感性的机制。本研究有助于阐明Gal-3促进卵巢癌发展和化疗耐药的机理，将为实现上皮性卵巢癌的精准治疗提供新的理论依据以及靶点。

Severe metastatic implants and chemotherapy resistance are two major causes for treatment failure in epithelial ovarian carcinoma (EOC), however, the specific mechanism is still not clear yet. In our previous study, we have found that Galectin-3 can have an influence on metastatic capability of ovarian cancer cells, and on chemotherapy sensitivity. By regulating the expression of Gal-3, β-catenin would change respectively. Moreover, there was a positive correlation in regards to the expressions of Gal-3 and β-catenin in the EOC tissues. These findings suggested that Gal-3 may function via the Wnt/β-catenin pathway in EOC。Based on our previous works, We will use Co-Immunoprecipitation, westernblot and immunofluorescence to explore the mechanism of Gal-3 regulation on metastatic capability, chemotherapy sensitivity through Wnt/β-Catenin. Nude mice of EOC model were used to verify the mechanism of Gal-3 regulation on metastatic capability, chemotherapy sensitivity. This study will help to clarify the mechanism of Gal-3 promoting metastatic capability and chemotherapy sensitivity in EOC, and it will provide new theoretical base and target for accurate treatment of EOC.