Prevention of the nuclear translocation of ANXA1 with Tat-NTS was recently reported to alleviate neuronal injury and protect against cerebral stroke. However, the role that Tat-NTS plays in the occurrence and development of gliomas still needs to be elucidated. Therefore, human glioblastoma (GB) cells were treated with various concentrations of Tat-NTS for 24 h, and cell proliferation, migration and invasion were assessed with CCK-8 and Transwell assays. The nuclear translocation of ANXA1 was evaluated by subcellular extraction and immunofluorescence, and protein expression levels were detected by Western blot analysis. In addition, the activity of MMP-2/9 was measured by gelatin zymography. The results revealed that Tat-NTS significantly inhibited the nuclear translocation of ANXA1 in U87 cells and inhibited the proliferation, migration and invasion of GB cells. Tat-NTS also suppressed cell cycle regulatory proteins and MMP-2/-9 activity and expression. Moreover, Tat-NTS reduced the level of p-p65 NF-κB in U87 cells. These results suggest that the Tat-NTS-induced inhibition of GB cell proliferation, migration and invasion is closely associated with the induction of cell cycle arrest, downregulation of MMP-2/-9 expression and activity and suppression of the NF-κB signaling pathway. Thus, Tat-NTS may be a potential chemotherapeutic agent for the treatment of GB.

最近有报道称，用 Tat-NTS 预防 ANXA1 的核易位可减轻神经元损伤并预防脑卒中。然而，Tat-NTS在胶质瘤发生发展中的作用仍有待阐明。因此，人胶质母细胞瘤 (GB) 细胞用不同浓度的 Tat-NTS 处理 24 小时，并用 CCK-8 和 Transwell 测定法评估细胞增殖、迁移和侵袭。通过亚细胞提取和免疫荧光评估ANXA1的核转位，并通过Western印迹分析检测蛋白质表达水平。此外，MMP-2/9的活性通过明胶酶谱法测定。结果表明，Tat-NTS显着抑制了U87细胞中ANXA1的核转位，抑制了GB细胞的增殖、迁移和侵袭。Tat-NTS 还抑制细胞周期调节蛋白和 MMP-2/-9 活性和表达。此外，Tat-NTS 降低了 U87 细胞中 p-p65 NF-κB 的水平。这些结果表明，Tat-NTS 诱导的 GB 细胞增殖、迁移和侵袭的抑制与诱导细胞周期停滞、下调 MMP-2/-9 表达和活性以及抑制 NF-κB 信号通路密切相关。 . 因此，Tat-NTS 可能是治疗 GB 的潜在化疗剂。