首页> 美国卫生研究院文献>Marine Drugs >The Inhibitory Effect of Propylene Glycol Alginate Sodium Sulfate on Fibroblast Growth Factor 2-Mediated Angiogenesis and Invasion in Murine Melanoma B16-F10 Cells In Vitro
【2h】

The Inhibitory Effect of Propylene Glycol Alginate Sodium Sulfate on Fibroblast Growth Factor 2-Mediated Angiogenesis and Invasion in Murine Melanoma B16-F10 Cells In Vitro

机译:丙二醇海藻酸钠硫酸钠对成纤维细胞生长因子2介导的血管生成和小鼠黑素瘤B16-F10细胞体外侵袭的抑制作用。

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

Melanoma is one of the most malignant and aggressive types of cancer worldwide. Fibroblast growth factor 2 (FGF2) is one of the critical regulators of melanoma angiogenesis and metastasis; thus, it might be an effective anti-cancer strategy to explore FGF2-targeting drug candidates from existing drugs. In this study, we evaluate the effect of the marine drug propylene glycol alginate sodium sulfate (PSS) on FGF2-mediated angiogenesis and invasion. The data shows that FGF2 selectively bound to PSS with high affinity. PSS inhibited FGF2-mediated angiogenesis in a rat aortic ring model and suppressed FGF2-mediated invasion, but not the migration of murine melanoma B16-F10 cells. The further mechanism study indicates that PSS decreased the expression of activated matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9), and also suppressed their activity. In addition, PSS was found to decrease the level of Vimentin in B16-F10 cells, which is known to participate in the epithelial–mesenchymal transition. Notably, PSS did not elicit any changes in cancer cell viability. Based on the results above, we conclude that PSS might be a potential drug to regulate the tumor microenvironment in order to facilitate the recovery of melanoma patients.
机译:黑色素瘤是全球最恶性和侵略性癌症之一。成纤维细胞生长因子2(FGF2)是黑色素瘤血管生成和转移的关键调节因子之一;因此,从现有药物中探索靶向FGF2的候选药物可能是一种有效的抗癌策略。在这项研究中,我们评估了海洋药物丙二醇海藻酸钠硫酸钠(PSS)对FGF2介导的血管生成和侵袭的影响。数据显示FGF2以高亲和力选择性结合至PSS。 PSS在大鼠主动脉环模型中抑制FGF2介导的血管生成,并抑制FGF2介导的侵袭,但不抑制鼠类黑素瘤B16-F10细胞的迁移。进一步的机理研究表明,PSS降低了激活的基质金属蛋白酶2(MMP-2)和基质金属蛋白酶9(MMP-9)的表达,并抑制了它们的活性。此外,发现PSS可以降低B16-F10细胞中波形蛋白的水平,已知该波形蛋白参与上皮-间质转化。值得注意的是,PSS并未引起癌细胞活力的任何变化。根据以上结果,我们得出结论,PSS可能是调节肿瘤微环境以促进黑色素瘤患者康复的潜在药物。

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