MAGE-A4是一种高表达于多种肿瘤细胞和正常睾丸组织的CT抗原，虽已有研究确定其MHD结构域可以与E3泛素连接酶的RING结构域相互作用，但目前为止对其功能研究还很少。PSMD10是由锚定重复序列翻译成的小分子癌蛋白，可通过不同的通路与多种蛋白发生相互作用，以激活转录或抑制细胞凋亡。现已知MAGE-A4和PSMD10存在相互作用，基于MAGE-A4在肿瘤细胞中的异常表达以及PSMD10在肿瘤发生过程中的特殊作用，我们猜测MAGE-A4功能的发挥可能与PSMD10相关。实验首先通过co-IP验证了两者的相互作用，再分别构建MAGE-A4和PSMD10高表达的质粒转入细胞后观察细胞的增殖和迁移。经初步探究发现MAGE-A4高表达时两种细胞增殖减少，迁移变慢；PSMD10高表达时MCF-7的迁移变快，但MAGE-A4同时高表达时，整体表现出对MCF-7的迁移影响不大。上述结果表明：MAGE-A4对MCF-7和HepGⅡ细胞的增殖和迁移都有抑制作用（P＜0.05）。PSMD10促进MCF-7细胞的迁移（P<0.05），而MAGE-A4会使PSMD10的作用受到抑制（P＜0.05）。这些结论为确定MAGE-A4发挥作用的通路提供了理论依据。

MAGE-A4 is a kind of CT antigens that only expresses in human testicular cells and multiple types of tumor cells. Although some research revealed that its MHD can interact with the RING domain of E3 ubiquitin ligase, the function of this protein is not clear so far. PSMD10 is a small oncoprotein that consists of cancer ankyrin repeats. It can interact with various proteins to activate transcription and suppress apoptosis through different signal pathways. It is reported that MAGE-A4 can interacts with PSMD10 via yeast two-hybrid system. Based on the abnormal expression of MAGE-A4 and the special effect of PSMD10 in tumor, we attempted to clarify the function of MAGE-A4 and explore whether it is related to PSMD10. We first validated that MAGE-A4 interacted with PSMD10 by co-IP. Then we constructed plasmid including two genes respectively and transfected them into cells and study their proliferation and migration. We found that when the expression of MAGE-A4 is high, both of MCF-7 and HepGⅡ proliferated and migrated slower. When the expression of PSMD10 is high, MCF-7 migrated more rapidly; however, when the expression of MAGE-A4 is high simultaneously, the migration of MCF-7 are not affected. The results demonstrated that MAGE-A4 inhibit cell proliferation and migration both in MCF-7 and HepGⅡ(P<0.05); while PSMD10 promote cell migration in MCF-7(P<0.05) and MAGE-A4 plays a role as an inhibitor that attenuates the function of PSMD10(P<0.05). These results provide theoretical support for finding out the pathways of MAGE-A4.