Wnt信号通路在神经胶质瘤的发生发展过程中发挥重要作用。PAX3作为胚胎干性基因在肿瘤发生发展过程中扮演重要角色。我们的前期研究已证实：PAX3在胶质瘤细胞和组织中高表达，其通过促进胶质瘤细胞增殖和侵袭，抑制凋亡而发挥癌基因作用，然而其发挥癌基因作用的具体分子机制不明确。预实验结果初步证实在胶质瘤U87细胞中PAX3与β-catenin蛋白表达负相关并且存在相互作用。据此我们提出假说：PAX3可能是通过调控Wnt/β-catenin信号通路在胶质瘤细胞中发挥癌基因作用。本课题拟通过基因沉默和过表达技术在细胞、组织和裸鼠水平采用一系列分子生物学实验技术研究PAX3通过介导Wnt信号通路调控神经胶质瘤细胞促增殖和抗凋亡等恶性生物学行为的具体分子机制。通过本项目的研究，阐明PAX3致癌的具体分子机制，为神经胶质瘤的发病机制研究提供实验基础，并为胶质瘤基因靶向治疗提供新的靶标。

Wnt/β-catenin signal pathway plays an important role in the pathogenesis and development of gliomas. As an embryonic stem cell gene, PAX3 plays an important role in the oncogenesis. In the our preliminary study, it has been demonstrated that PAX3 is highly expressed in glioma, and that it promotes proliferation and invasion of glioma cells, and suppresses tumor apoptosis, thereby playing an oncogene-like role. However, the defined molecular mechanism of PAX3 regulating proliferation, invasion and apoptosis of glioma cells remain largely unknown. Furthermore, our previous research has demonstrated that β-catenin expression was dramatically down-regulated after PAX3 expression was suppressed by siRNA; The interactions between PAX3 and β-catenin were detected with co-immunoprecipitation. Therefore we propose a hypothesis: PAX3 plays an oncogene role by regulating the Wnt/β-catenin signaling pathways in glioma cells. In this study, we introduce the related molecular biological techniques in the level of cells, tissues and nude mice, such as gene silencing and plasmid overexpression technique, and aim to investigate the specific molecular mechanism of PAX3 regulating the malignant biological behaviors of glioma via Wnt/β-catenin signal pathway. This study may provide theoretical support and innovative clinical thoughts for the study on pathogenesis and target therapy of glioma.