AKT2 的表达与胶质瘤的恶性进展相关，并且对于细胞的存活和侵袭是必需的。

AKT2 expression is associated with glioma malignant progression and required for cell survival and invasion.

机构信息

Department of Neurosurgery, Tianjin Medical University General Hospital and Laboratory of Neuro-Oncology, Tianjin Neurological Institute, Tianjin 300052, P.R. China.

出版信息

Oncol Rep. 2010 Jul;24(1):65-72. doi: 10.3892/or_00000829.

DOI:10.3892/or_00000829

PMID:20514445

Abstract

Recent data suggest that AKT2, one of AKT isoforms, plays an important role in tumorigenesis of human cancers. However, little evidence exists to show the mechanism of AKT2 involved in tumorigenesis. In this study, we show that AKT2 protein expression increased significantly in high grade gliomas in comparison to low grade gliomas and correlated with the expression of NFkappaB, BCL2, MMP2 and MMP9 by immunostaining. Further, down-regulation of AKT2 expression by antisense AKT2 induced glioma cell apoptosis mediated by NFkappaB and BCL2. In addition, decreased MMP2 and MMP9 expression in AKT2 knocked-down glioma cells was subsequently detected, consistent with the decreased invasion. These findings indicate that AKT2 expression is associated with more advanced and especially aggressive gliomas and critical for cell survival and invasion.

摘要

最近的数据表明，AKT 同工酶之一 AKT2 在人类癌症的肿瘤发生中发挥着重要作用。然而，目前几乎没有证据表明 AKT2 参与肿瘤发生的机制。在这项研究中，我们通过免疫染色发现 AKT2 蛋白表达在高级别神经胶质瘤中显著增加，与 NFkappaB、BCL2、MMP2 和 MMP9 的表达相关。此外，通过反义 AKT2 下调 AKT2 表达可诱导 NFkappaB 和 BCL2 介导的神经胶质瘤细胞凋亡。另外，在 AKT2 敲低的神经胶质瘤细胞中检测到 MMP2 和 MMP9 表达减少，与侵袭减少一致。这些发现表明 AKT2 的表达与更高级别、更具侵袭性的神经胶质瘤相关，对细胞存活和侵袭至关重要。