丙泊酚通过miR-301a/PI3K/AKT轴调控胶质瘤细胞增殖、迁移和侵袭
Propofol regulates proliferation,migration and invasion of glioma cells through miR-301a/PI3K/AKT axis
黄德勋 1周晋1
作者信息
- 1. 629000 四川,遂宁市第一人民医院麻醉科
- 折叠
摘要
目的 探讨丙泊酚在脑胶质瘤(glioblastoma,GBM)中的作用及其潜在机制.方法 细胞计数试剂盒-8(CCK-8)和克隆形成实验测定细胞增殖.Transwell检测细胞凋亡和迁移、侵袭.生信数据库和qRT-PCR分析miR-301a的水平.蛋白印迹法分析PI3K/AKT通路活性.结果 丙泊酚抑制GBM细胞增殖、迁移和侵袭,促进细胞凋亡.miR-301a在GEB组织和细胞中表达上调.丙泊酚通过抑制miR-301a的表达抑制GBM细胞的恶性进展.此外,miR-301a过表达可以促进p-PI3K和p-AKT的蛋白表达,而丙泊酚处理部分减弱miR-301a过表达对p-PI3K和p-AKT表达的促进作用.结论 丙泊酚通过可能介导miR-301a/PI3K/AKT轴抑制GBM进展,这项研究有助于指导临床使用丙泊酚,以期在手术切除肿瘤后获得更好的患者预后.
Abstract
Objective To investigate the role of propofol in glioblastoma(GBM)and its underlying mechanisms.Methods Cell proliferation was determined by cell counting Kit-8(CCK-8)and clone formation assay.Transwell assay for apoptosis and migration,invasion.Bioconfidence database and qRT-PCR were used to analyze the level of miR-301a.Protein immunoblotting was used to analyze PI3K/AKT pathway activity.Results Propofol inhibits GBM cell proliferation,migration and invasion and promotes apoptosis.miR-301a expression is upregulated in GEB tissues and cells.Propofol inhibited the malignant progression of GBM cells by suppressing miR-301a expression.In addition,miR-301a overexpression promoted the protein expression of p-P13K and p-AKT,whereas propofol treatment partially attenuated the promotional effect of miR-301a overexpression on the expression of p-P13K and p-AKT.Conclusion Propofol inhibits GBM progression by potentially mediating the miR-301a/PI3K/AKT axis,and this study could help guide the clinical use of propofol with a view to obtaining a better patient prognosis after surgical removal of the tumor.
关键词
丙泊酚/miR-301a/PI3K/AKT通路/胶质瘤/增殖/迁移Key words
Propofol/miR-301a/PISK/AKT pathway/Glioblastoma/Proliferation,/Migration引用本文复制引用
出版年
2025
NETL
NSTL
万方数据