首页> 美国卫生研究院文献>Oncology Letters >Luteolin reduces migration of human glioblastoma cell lines via inhibition of the p-IGF-1R/PI3K/AKT/mTOR signaling pathway
【2h】

Luteolin reduces migration of human glioblastoma cell lines via inhibition of the p-IGF-1R/PI3K/AKT/mTOR signaling pathway

机译:木犀草素通过抑制p-IGF-1R / PI3K / AKT / mTOR信号通路减少人胶质母细胞瘤细胞系的迁移

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Luteolin (3′,4′,5,7-tetrahydroxyflavone) is a common dietary flavonoid, which has been demonstrated to exert anticancer effects in multiple cancer models. However, the detailed mechanisms underlying the inhibitory effect of luteolin on glioblastoma cell metastasis remain poorly understood. The present study assessed the effects of luteolin in the U251MG and U87MG human glioblastoma cell lines. Luteolin treatment significantly inhibited glioblastoma cell migration, and this effect was associated with downregulated matrix metalloproteinase (MMP)-2, MMP-9 and upregulated tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2. In addition, luteolin also inhibited the epithelial-mesenchymal transition-associated phenotype. Furthermore, the phosphorylated insulin-like growth factor-1 receptor/phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin (p-IGF-1R/PI3K/AKT/mTOR) signaling pathway was demonstrated to participate in these processes. The results of the present study demonstrated that the flavonoid luteolin reduced the migration of glioblastoma cells by altering p-IGF-1R/PI3K/AKT/mTOR activation, and may have potential applications for chemoprevention in a clinical setting.
机译:木犀草素(3',4',5,7-四羟基黄酮)是一种常见的饮食类黄酮,已被证明在多种癌症模型中均具有抗癌作用。但是,对木犀草素抑制胶质母细胞瘤细胞转移的潜在作用的详细机制仍知之甚少。本研究评估了木犀草素在U251MG和U87MG人胶质母细胞瘤细胞系中的作用。木犀草素治疗显着抑制胶质母细胞瘤细胞迁移,这种作用与基质金属蛋白酶(MMP)-2,MMP-9的下调以及金属蛋白酶组织的抑制剂(TIMP)-1和TIMP-2的上调有关。此外,木犀草素还抑制上皮-间质转化相关表型。此外,已证明磷酸化的胰岛素样生长因子-1受体/磷​​酸肌醇3激酶/蛋白激酶B /雷帕霉素的哺乳动物靶标(p-IGF-1R / PI3K / AKT / mTOR)信号通路参与了这些过程。本研究的结果表明,黄酮类木犀草素通过改变p-IGF-1R / PI3K / AKT / mTOR激活来减少胶质母细胞瘤细胞的迁移,并且在临床上可能具有化学预防的潜在应用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号