前期研究表明NAP1L1在胶质瘤中高表达，干扰胶质瘤细胞中NAP1L1的表达后细胞的增殖、侵袭和迁移能力显著被抑制。同时干扰胶质瘤细胞中NAP1L1的表达后PI3K/Akt通路的关键分子p-PI3K和p-Akt均显著下调。进一步免疫共沉淀提示HDGF蛋白可能是NAP1L1的候选直接相互作用蛋白。干扰NAP1L1可以抑制HDGF蛋白表达但不影响mRNA的表达，而蛋白质赖氨酸数据库发现HDGF有多个泛素化位点。此外，有研究显示HDGF可以通过PI3K/Akt通路促进胶质瘤细胞的EMT。据此推测NAP1L1在胶质瘤中可能通过与HDGF直接相互作用并抑制其泛素化降解，通过PI3K/Akt通路促进了胶质瘤细胞的EMT。进一步工作围绕NAP1L1和HDGF的相互关系展开，并进一步验证两者在胶质瘤中的功能、表达及与预后的关系。本课题若进展顺利，将为阐明胶质瘤发生及发展的分子机制提供一个新的思路。

NAP1L1 was overexpressed in glioma tissues, and knockdown of NAP1L1 inhibited glioma cell proliferation, invasion and migration. Moreover, silence of NAP1L1 inactivated PI3K/Akt pathway. Further Co-IP assay suggested HDGF may be the interacting protein of NAP1L1. Knockdown of NAP1L1 silenced the protein level of HDGF but not effect on mRNA level, and multiple sites of ubiquitination were identified by analyzing with Compendium of Protein Lysine Modifications database. Thus, NAP1L1 might sustain high expression of HDGF by inhibiting ubiquitination of HDGF. Besides, previous study confirmed HDGF promoted glioma cell growth, invasion and migration through PI3K/Akt pathway. Consequently, we supposed NAP1L1 mediates HDGF by protein interaction, and promotes glioma cell growth, invasion and migration through PI3K/Akt pathway. Subsequent study mainly focused on the regulating relationship between NAP1L1 and HDGF, as well as their cellular function in glioma. These findings will provide a new sight for clarifying the molecular mechanism of glioma development.