全反式维甲酸抑制U87细胞血管生成拟态的机制研究

凌耿强; 马东营; 何瑞星; 王悦娜; 叶伟

doi:10.3971/j.issn.1000-8578.2017.16.1470

全反式维甲酸抑制U87细胞血管生成拟态的机制研究

Mechanism of All-trans Retinoic Acid Inhibiting Vasculogenic Mimicry Formation in Glioma Cell Line U87

摘要

摘要:
目的探讨全反式维甲酸（all-trans retinoic acid, ATRA）抑制U87胶质瘤细胞血管生成拟态（VM）的机制。
方法通过在细胞培养液中加入不同浓度的ATRA作用于U87细胞，利用三维培养及管道计数实验、侵袭小室实验、Western blot、明胶酶谱等方法，比较组间U87细胞的VM形成能力、细胞侵袭能力、NF-κB蛋白磷酸化程度、MMP-2活性的差别。
结果随着培养液中ATRA浓度逐渐增高，U87细胞形成VM的能力、细胞侵袭力、NF-κB蛋白磷酸化程度及MMP-2活性均逐渐减弱。
结论 ATRA的下游信号通路NF-κB受到抑制导致MMP-2活性下降，从而使细胞侵袭力下降，这可能是ATRA抑制U87细胞VM形成的内在机制之一。

Abstract:
Objective To investigate the mechanism of all-trans retinoic acid (ATRA) inhibiting vasculogenic mimicry (VM) formation in glioma cell line U87.
Methods We added different concentration of ATRA into U87 culture medium, in order to compare the VM forming ability, invading ability, NF-κB phosphorylation capacity and MMP-2 activity among groups via Tube formation tests, Transwell tests, Western blot tests and Zymography tests.
Results Along with the elevation of ATRA concentration, the VM forming ability, invading ability, NF-κB phosphorylation capacity and MMP-2 activity all became weakened.
Conclusion The mechanism of ATRA inhibiting VM formation in glioma cell line U87 might be due to the weakened cell invading ability, which was caused by decreased MMP-2 activity resulted from down-regulation of NF-κB signaling pathways.

HTML全文

参考文献(18)

施引文献

资源附件(0)