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维甲酸酰胺通过激活Akt信号通路抑制LN-308胶质瘤细胞的增殖和迁移。

Inhibition of LN-308 glioma cell proliferation and migration by retinoic acid amide through activation of Akt pathway.

作者信息

Zhu Jun, Lu Xiang-Dong, Si Feng, Song Chun-Yu, Meng Qing-Hai

机构信息

Department of Neurosurgery, Brain Hospital, Affiliated Hospital of Qingdao UniversityQingdao, China; Department of Neurosurgery, People's Hospital of Laiwu CityLaiwu, China.

Department of Neurosurgery, People's Hospital of Laiwu City Laiwu, China.

出版信息

Int J Clin Exp Pathol. 2015 Nov 1;8(11):13921-7. eCollection 2015.

Abstract

The present study was performed to investigate the effect of retinoic acid amide (RAA) on the expression of integrin α3β1, rate of cell proliferation and migration in p53-deficient glioma cell line, LN-308. The results revealed promotion of integrin α3 expression, reduction in proliferation and migration in RAA treated cells compared to the control LN-308 glioma cells. Promotion of RAA induced integrin α3β1 expression led to the enhancement in cyclin-dependent kinase nuclear localization and activation of Akt pathway. In addition, RAA treatment inhibited the expression of nuclear factor-κB, Bcl-2 and epidermal growth factor receptor (EGFR). These factors are responsible for promoting the rate of cell proliferation and survival in the carcinoma cells. Thus RAA treatment inhibits rate of LN-308 glioma cell proliferation and migration through increase in integrin α3β1 expression and activation of Akt pathway. Therefore, RAA can be of therapeutic importance for the treatment of glioma.

摘要

本研究旨在探讨维甲酸酰胺(RAA)对p53基因缺失的胶质瘤细胞系LN-308中整合素α3β1表达、细胞增殖速率及迁移的影响。结果显示,与对照LN-308胶质瘤细胞相比,RAA处理的细胞中整合素α3表达增加,增殖和迁移减少。RAA诱导的整合素α3β1表达增加导致细胞周期蛋白依赖性激酶核定位增强及Akt通路激活。此外,RAA处理抑制了核因子κB、Bcl-2和表皮生长因子受体(EGFR)的表达。这些因子负责促进癌细胞的增殖速率和存活。因此,RAA处理通过增加整合素α3β1表达和激活Akt通路来抑制LN-308胶质瘤细胞的增殖和迁移速率。所以,RAA对胶质瘤治疗可能具有重要的治疗意义。

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