We aimed to explore the role of capillary morphogenetic protein 2 (CMG2) in glioma cell invasion and the possible molecular mechanism. Glioma cells U87 and U251 stably overexpressing CMG2 were constructed by lentiviral transfection. The changes of cell invasion and migration were tested by Matrigel-transwell assay and scratch assay, respectively. A mouse model with orthotopically transplanted tumour was established to evaluate the effects of CMG2 overexpression on the in vivo invasion of glioma cells and survival time. The differences of filopodia and lamellar pseudopodia among glioma cells with different CMG2 expressions were observed by immunofluorescence assay. The expressions of YAP and p-YAP in glioma cells overexpressing CMG2 or not were compared by Western blot. Compared with the control group, overexpression of CMG2 enhanced the invasion and migration capacities of glioma cells (p < 0.05). The tumour tissues of mice transplanted with glioma cells overexpressing CMG2 were obviously invaded, and their survival time was significantly shortened (p < 0.05). Immunofluorescence staining showed that glioma cells overexpressing CMG2 formed more lamellipodia and filopodia than those of the control group. As glioma cells overexpressing CMG2 formed more pseudopodia, the expression of YAP, a key effector protein of the Hippo pathway, was up-regulated. CMG2 promoted the invasion of glioma cells, and may induce pseudopodium formation by up-regulating YAP expression.

中文翻译：

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毛细管形态发生蛋白2对神经胶质瘤细胞侵袭的促进作用及其分子机制。

我们旨在探讨毛细血管形态发生蛋白2（CMG2）在胶质瘤细胞侵袭中的作用以及可能的分子机制。通过慢病毒转染构建稳定表达CMG2的胶质瘤细胞U87和U251。分别通过Matrigel-transwell测定法和刮擦测定法测试细胞侵袭和迁移的变化。建立了具有原位移植肿瘤的小鼠模型，以评估CMG2过表达对神经胶质瘤细胞体内侵袭和存活时间的影响。免疫荧光法观察不同CMG2表达的神经胶质瘤细胞中丝状伪足和片状伪足的差异。通过蛋白质印迹比较了过表达或未过表达CMG2的神经胶质瘤细胞中YAP和p-YAP的表达。与对照组相比，CMG2的过表达增强了胶质瘤细胞的侵袭和迁移能力（p <0.05）。移植了过量表达CMG2的神经胶质瘤细胞的小鼠的肿瘤组织明显侵袭，其生存时间明显缩短（p <0.05）。免疫荧光染色显示，与对照组相比，过表达CMG2的神经胶质瘤细胞形成了更多的片状脂蛋白和丝状伪足。由于过表达CMG2的神经胶质瘤细胞形成更多的伪足，因此上调了HAP途径的关键效应蛋白YAP的表达。CMG2促进神经胶质瘤细胞的侵袭，并可能通过上调YAP表达诱导假pseudo形成。并且它们的生存时间显着缩短（p <0.05）。免疫荧光染色显示，与对照组相比，过表达CMG2的神经胶质瘤细胞形成了更多的片状脂蛋白和丝状伪足。随着过表达CMG2的神经胶质瘤细胞形成更多的假足，YAP的表达被上调，YAP是河马途径的关键效应蛋白。CMG2促进神经胶质瘤细胞的侵袭，并可能通过上调YAP表达诱导假pseudo形成。并且它们的生存时间显着缩短（p <0.05）。免疫荧光染色显示，与对照组相比，过表达CMG2的神经胶质瘤细胞形成了更多的片状脂蛋白和丝状伪足。由于过表达CMG2的神经胶质瘤细胞形成更多的伪足，因此上调了HAP途径的关键效应蛋白YAP的表达。CMG2促进神经胶质瘤细胞的侵袭，并可能通过上调YAP表达诱导假pseudo形成。