HIV-1病毒蛋白R下调胶质母细胞瘤U87MG细胞中的Ebp1并使p53稳定。
HIV-1 viral protein R downregulates Ebp1 and stabilizes p53 in glioblastoma U87MG cells.
作者信息
Zhang S, Zhang B, Xu X, Wang L, Feng X, Wang Q, Huang H, Wu J, Li P, Wang J
机构信息
Tianjin Neurosurgical Institute, Tianjin Huanhu Hospital, Tianjin, 300060, People's Republic of China.
出版信息
Clin Transl Oncol. 2014 Mar;16(3):293-300. doi: 10.1007/s12094-013-1072-7. Epub 2013 Jul 5.
PURPOSE
HIV-1 viral protein R (Vpr) inhibits cell growth and induces apoptosis in a wide range of cancers. However, the mechanism by which Vpr induces cell cycle arrest and apoptosis in GBM cell lines is unclear. The present work was taken to detect the proteins interacted with Vpr in U87MG cells.
METHODS
We analyzed the differential expression of proteins between glioblastoma cell U87MG treated with Ad-Vpr and untreated by 2-DE. We used antibody array analysis to analyze the common molecules in the apoptosis of U87MG induced by Vpr.
RESULTS
We analyzed the differential expression of proteins between U87MG cell treated with Ad-Vpr and untreated, and found that proteins related to DNA damage repair or different apoptosis pathways were involved in the G2 arrest and apoptosis mediated by Vpr. In addition, proliferation-associated protein 2G4 (PA2G4), also known as Ebp1, was down-regulated and p53 was up-regulated in U87MG cells treated with Ad-Vpr.
CONCLUSIONS
Our data suggest that Vpr may inhibit Ebp1 to stabilize p53, which in turn leads to G2 arrest and apoptosis in U87MG cells.
目的
HIV-1病毒蛋白R（Vpr）可抑制多种癌症中的细胞生长并诱导细胞凋亡。然而，Vpr在胶质母细胞瘤细胞系中诱导细胞周期停滞和细胞凋亡的机制尚不清楚。本研究旨在检测U87MG细胞中与Vpr相互作用的蛋白质。
方法
我们通过二维电泳分析了经腺病毒载体Vpr（Ad-Vpr）处理的胶质母细胞瘤细胞U87MG与未处理细胞之间蛋白质的差异表达。我们使用抗体芯片分析来分析Vpr诱导的U87MG细胞凋亡中的共同分子。
结果
我们分析了经Ad-Vpr处理的U87MG细胞与未处理细胞之间蛋白质的差异表达，发现与DNA损伤修复或不同凋亡途径相关的蛋白质参与了Vpr介导的G2期停滞和细胞凋亡。此外，在经Ad-Vpr处理的U87MG细胞中，增殖相关蛋白2G4（PA2G4），也称为Ebp1，表达下调，而p53表达上调。
结论
我们的数据表明，Vpr可能通过抑制Ebp1来稳定p53，进而导致U87MG细胞发生G2期停滞和细胞凋亡。
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