VE-他汀/Egfl7小干扰RNA在体外抑制恶性胶质瘤血管生成。
VE-statin/Egfl7 siRNA inhibits angiogenesis in malignant glioma in vitro.
作者信息
Huang Chunhai, Yuan Xianrui, Li Zhao, Tian Zhi, Zhan Xianquan, Zhang Jingjing, Li Xuejun
机构信息
Department of Neurosurgery, First Affiliated Hospital of Jishou University Jishou 416000, Hunan.
Department of Neurosurgery, Xiangya Hospital, Central South University Changsha 410008, Hunan, China ; The Institute of Skull Base Surgery and Neurooncology at Hunan Changsha 410008, Hunan, China.
出版信息
Int J Clin Exp Pathol. 2014 Feb 15;7(3):1077-84. eCollection 2014.
This study investigated the role of VE-statin/Egfl7 and its mechanism in angiogenesis in malignant glioma. Transwell culture plates were used to establish an U251-HUVEC co-culture system, which was used to mimic the interaction between malignant glioma and endothelial cells. Lentiviral vectors expressing VE-statin/Egfl7 siRNA were constructed, and U251 cells and HUVECs were transfected to inhibit VE-statin/Egfl7 expression. The proliferation, adherence, migration, and lumen formation of endothelial cells were assayed to investigate the influence of VE-statin/Egfl7 on angiogenesis in malignant glioma in vitro. Data showed that HUVEC growth was temporarily slowed after silencing the VE-statin/Egfl7 gene but rapidly returned to normal. Although endothelial cell migration was not influenced, cell adherence was markedly inhibited. Furthermore, the endothelial cells failed to generate a capillary-like lumen after VE-statin/Egfl7 gene silencing. Therefore, it can be concluded that VE-statin/Egfl7 may regulate the adherence of endothelial cells, thus playing an important role in endothelium-induced lumen formation during angiogenesis in malignant glioma.
本研究探讨了VE-他汀/Egfl7在恶性胶质瘤血管生成中的作用及其机制。采用Transwell培养板建立U251-HUVEC共培养体系，以模拟恶性胶质瘤与内皮细胞之间的相互作用。构建表达VE-他汀/Egfl7 siRNA的慢病毒载体，并转染U251细胞和HUVECs以抑制VE-他汀/Egfl7的表达。检测内皮细胞的增殖、黏附、迁移及管腔形成，以研究VE-他汀/Egfl7对恶性胶质瘤血管生成的体外影响。数据显示，沉默VE-他汀/Egfl7基因后，HUVEC生长暂时减慢，但迅速恢复正常。虽然内皮细胞迁移未受影响，但细胞黏附明显受到抑制。此外，VE-他汀/Egfl7基因沉默后，内皮细胞未能形成毛细血管样管腔。因此，可以得出结论，VE-他汀/Egfl7可能调节内皮细胞的黏附，从而在恶性胶质瘤血管生成过程中内皮诱导的管腔形成中发挥重要作用。
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