胶质母细胞瘤是星形细胞来源肿瘤中异质性最高的肿瘤类型，其中瘤巨细胞参与胶质母细胞瘤发生发展，但形成机制尚不清楚。我们前期发现毛细血管形成因子CMG2在胶质瘤中高表达，降低CMG2表达导致胞质分裂受阻，形成瘤巨细胞，细胞侵袭能力下降，但CMG2参与胶质瘤胞质分裂，瘤巨细胞形成及侵袭的具体机制尚不清楚。细胞骨架蛋白F-actin在胞质分裂及细胞运动中起着重要作用，前期研究发现CMG2与F-actin能够在胶质瘤细胞边缘处发生共定位，因此我们推测CMG2通过与F-actin发生相互作用调控F-actin在胶质瘤细胞中的分布，进而控制胶质瘤胞质分裂，缺乏CMG2时，胞质分裂失败，形成瘤巨细胞，并进一步影响细胞侵袭迁移能力。本项目拟通过细胞生物学及分子生物学技术证实以上研究假设，了解CMG2在胶质瘤瘤巨细胞形成及侵袭中的作用机制，将为胶质瘤的有效治疗及病人预后的判断提供理论基础。

Glioblastoma is the most heterogeneous cancers, which originate from astrocyte. Polyploid giant cancer cells often observed in the sections of glioblastoma patients are related with the development of glioblastoma, but the mechanisms of the PGCCs formation are largely undefined. In our previous study, Capillary morphogenesis gene 2 (CMG2) was found to be highly expressed in glioma cells. The knockdown of CMG2 interfered with glioma cells cytokinesis and was associated with the formation of PGCCs whose invasion was remarkably suppressed. But the mechanism of CMG2 in glioma cell cytokinesis and invasion were largely unknown. Cytoskeleton F-actin was involved in cytokinesis and cell motility, and our previous study showed that CMG2 and F-actin colocalized in the cell edge. So in this study, we suppose that the existence of intricate interactions between CMG2 and F-actin regulate the array of F-actin in glioma cells, control cytokinesis and promote the invasion of glioma cell. Lack of CMG2 resulted in the failure of cytokinesis(formation of PGCCs) and inhibited the invasion of glioma. The technology of cell biology and molecular biology were both carried out to prove our hypothesis. The knowledge of our study could provide the theoretical framework for effective therapeutic strategies of glioblastoma and the prediction of patient prognosis.