ADAM10是一类影响细胞的侵袭迁移的重要因子。通过裂解多种重要蛋白分子，ADAM10参与了多条细胞内关键调控通路，但其在侵袭性垂体瘤中具体作用仍知之甚少。课题组前期首次证实ADAM10在侵袭性垂体瘤中特别是在高级别垂体瘤中表达明显升高，并且进一步通过细胞水平验证了钙调蛋白的抑制及src激酶的激活调控ADAM10介导细胞粘附蛋白CD44、L1裂解，但具体机制仍有待于进一步研究。本项目拟在前期基础上，进一步并利用慢病毒RNA干扰、蛋白芯片、组织芯片、免疫共沉淀、免疫组化、RT-PCR等技术，深入阐明ADAM10在侵袭性垂体腺瘤中裂解下游蛋白的具体调控机制。进而分析通路关键因子以及血液中其底物裂解片段表达对侵袭性垂体腺瘤临床特征的指示意义。为临床提供肿瘤分级，评估预后、制定治疗方案的实验依据，具有显著的临床意义。

ADAM10 is a factor which has effect on cell invasion and migration.ADAM10 is involved in many key pathways in cells via shedding a lot of important proteins and moleculars.In previous study, we revealed that ADAM10 is overexpression in invasive pituitary adenoma, especially in high-grade pituitary adenoma.Further we found that CaM is an inhibitor of ADAM10 in shedding CD44 and L1,when src kinase was played as a promotor.But the definite mechanism is not clear. In this project，we will explore the regulation of ADAM10 in cleaving its downstreaming moleculars CD44 and L1. Further we will analyze the key factor in this pathway and detect expression of solube fragment of CD44 and L1 in serum. Combined with the clinical data, we will measure the association between ADAM10 expression in pituitary adenoma and the clinical features.To provide a new marker for clinical diagnosis and treatments, in future clinical decisions, this study will be notably significant.