Brain and Spinal Cord Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Department of Tissue Engineering and Applied Cell Sciences, Faculty of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mol Neurobiol. 2018 Mar;55(3):2102-2110. doi: 10.1007/s12035-017-0445-2. Epub 2017 Mar 10.
Glioblastoma multiform (GBM) is a primary malignant brain tumor with a few therapeutic targets available for it. The interaction between the immune system and glioma is an important factor that could lead to novel therapeutic approaches to fight glioma. In this study, we investigated in vitro anti-inflammatory and apoptotic activity of atorvastatin in different concentrations 1, 5, and 10 μM on glioma spheroid cells cultured in a three-dimensional model in fibrin gel that indicate the complex in vivo microenvironment better than a simple two-dimensional cell culture. A mechanistic insight into the role of IL-17RA, TRAF3IP2, and apoptotic genes in progression of glioma could provide an important way for therapy of malignant tumors with manipulation of this inflammatory axis. To reach for these aims, after 24 and 48 h exposure with different concentrations of atorvastatin, caspase-8, caspase-3, Bcl-2, TRAF3IP2, and IL-17RA gene expression were assayed. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay and cell cycle assay were used for evaluating the cell apoptosis and proliferation. The results showed that atorvastatin has anti-inflammatory and apoptotic effects against glioma spheroids. Atorvastatin induced the expression of caspase-3 and caspase-8 and downregulated the expression of Bcl-2, TRAF3IP2, and IL-17RA especially at 10 μM concentration. These effects are dose dependent. The most likely mechanisms are the inhibition of inflammation by IL-17RA interaction with TRAF3IP2 and NF-κB signaling pathway. Finally, these results suggest that atorvastatin could be used as an anti-cancer agent for glioblastoma treatment.
胶质母细胞瘤(GBM)是一种原发性恶性脑肿瘤,目前只有少数治疗靶点可用。免疫系统与神经胶质瘤的相互作用是一个重要因素,可能导致针对神经胶质瘤的新的治疗方法。在这项研究中,我们在纤维蛋白凝胶中三维培养的胶质瘤球状体细胞中,研究了不同浓度(1、5 和 10μM)阿托伐他汀的体外抗炎和凋亡活性,该模型比简单的二维细胞培养更能模拟体内复杂的微环境。深入了解 IL-17RA、TRAF3IP2 和凋亡基因在神经胶质瘤进展中的作用,可能为通过操纵这一炎症轴治疗恶性肿瘤提供重要途径。为了达到这些目的,在暴露于不同浓度阿托伐他汀 24 和 48 小时后,检测了 caspase-8、caspase-3、Bcl-2、TRAF3IP2 和 IL-17RA 基因的表达。末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记法和细胞周期法用于评估细胞凋亡和增殖。结果表明,阿托伐他汀对神经胶质瘤球体具有抗炎和促凋亡作用。阿托伐他汀诱导 caspase-3 和 caspase-8 的表达,并下调 Bcl-2、TRAF3IP2 和 IL-17RA 的表达,特别是在 10μM 浓度下。这些作用呈剂量依赖性。最可能的机制是通过 IL-17RA 与 TRAF3IP2 相互作用和 NF-κB 信号通路抑制炎症。最后,这些结果表明,阿托伐他汀可用于胶质母细胞瘤的治疗。