少突胶质细胞通过血管生成素-2信号通路上调胶质母细胞瘤细胞的侵袭活性。
Oligodendrocytes Up-regulate the Invasive Activity of Glioblastoma Cells the Angiopoietin-2 Signaling Pathway.
作者信息
Kawashima Toshiyuki, Yashiro Masakazu, Kasashima Hiroaki, Terakawa Yuzo, Uda Takehiro, Nakajo Kosuke, Umaba Ryoko, Tanoue Yuta, Tamrakar Samantha, Ohata Kenji
机构信息
Department of Neurosurgery, Osaka City University Graduate School of Medicine, Osaka, Japan.
Molecular Oncology and Therapeutics, Osaka City University Graduate School of Medicine, Osaka, Japan
出版信息
Anticancer Res. 2019 Feb;39(2):577-584. doi: 10.21873/anticanres.13150.
BACKGROUND/AIM: Glioblastoma (GBM) is one of the most lethal solid cancers due to its highly invasive nature. The malignant potential of GBM cells might be partially regulated by surrounding normal cells, such as oligodendrocytes or fibroblasts. The aim of this study was to examine the interaction between stromal cells and GBM cells.
MATERIALS AND METHODS
Two GBM cell lines were used. The effect of stromal cells, oligodendrocytes or fibroblasts, on the invasive ability of GBM cells was examined by wound-healing assay and invasion assay.
RESULTS
Oligodendrocytes, in contrast to fibroblasts, significantly increased the migration and invasive ability of GBM cells. Angiopoietin-2 levels were high in the conditioned medium obtained from oligodendrocytes. Angiopoietin-2 significantly increased the motility of GBM, and the motility-stimulating activity of the oligodendrocytes-derived conditioned medium was significantly decreased by anti-angiopoietin-2-neutralizing antibody.
CONCLUSION
Glioma stromal cells, oligodendrocytes, might up-regulate the invasiveness of GBM cells via angiopoietin-2 signaling.
背景/目的：胶质母细胞瘤（GBM）因其高度侵袭性而成为最致命的实体癌之一。GBM细胞的恶性潜能可能部分受周围正常细胞（如少突胶质细胞或成纤维细胞）的调控。本研究旨在探讨基质细胞与GBM细胞之间的相互作用。
材料与方法
使用两种GBM细胞系。通过伤口愈合试验和侵袭试验检测基质细胞（少突胶质细胞或成纤维细胞）对GBM细胞侵袭能力的影响。
结果
与成纤维细胞相比，少突胶质细胞显著提高了GBM细胞的迁移和侵袭能力。从少突胶质细胞获得的条件培养基中血管生成素-2水平较高。血管生成素-2显著增加了GBM的运动性，抗血管生成素-2中和抗体显著降低了少突胶质细胞衍生的条件培养基的运动刺激活性。
结论
胶质瘤基质细胞少突胶质细胞可能通过血管生成素-2信号上调GBM细胞的侵袭性。
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