Qing-yue Ma , Xiao-yan Xu , Yuan-zhang Zhu, Ning-ning Yao, Yi-chong Liu, Xiao-di Gao, Qian Zhang, Wen-juan Luo
{"title":"Artesunate inhibits vasculogenic mimicry in choroidal melanoma through HIF-1 α/ VEGF/PDGF pathway","authors":"Qing-yue Ma , Xiao-yan Xu , Yuan-zhang Zhu, Ning-ning Yao, Yi-chong Liu, Xiao-di Gao, Qian Zhang, Wen-juan Luo","doi":"10.1016/j.acthis.2024.152174","DOIUrl":null,"url":null,"abstract":"<div><p>Choroidal melanoma (CM), a highly metastatic eye tumor, exhibits vasculogenic mimicry (VM) facilitated by hypoxia-induced angiogenesis. This study explored the inhibitory impact of the anti-malarial drug Artesunate (ART) on CM VM through modulation of the HIF-1α/VEGF/PDGF pathway. Immunohistochemistry (IHC) confirmed VM in CM with elevated VEGF and PDGF expression. Hypoxia promoted CM proliferation, upregulating HIF-1α, VEGF and PDGF. VEGF and PDGF enhanced CM migration, invasion and VM, with HIF-1α playing a crucial role. ART mitigated VM formation by suppressing the HIF-1α/VEGF/PDGF pathway, highlighting its potential as an anti-tumor agent in CM.</p></div>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0065128124000424","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 0
Abstract
Choroidal melanoma (CM), a highly metastatic eye tumor, exhibits vasculogenic mimicry (VM) facilitated by hypoxia-induced angiogenesis. This study explored the inhibitory impact of the anti-malarial drug Artesunate (ART) on CM VM through modulation of the HIF-1α/VEGF/PDGF pathway. Immunohistochemistry (IHC) confirmed VM in CM with elevated VEGF and PDGF expression. Hypoxia promoted CM proliferation, upregulating HIF-1α, VEGF and PDGF. VEGF and PDGF enhanced CM migration, invasion and VM, with HIF-1α playing a crucial role. ART mitigated VM formation by suppressing the HIF-1α/VEGF/PDGF pathway, highlighting its potential as an anti-tumor agent in CM.
脉络膜黑色素瘤(CM)是一种高度转移性眼部肿瘤,在缺氧诱导的血管生成作用下表现出血管生成模拟(VM)。本研究探讨了抗疟疾药物青蒿琥酯(ART)通过调节 HIF-1α/VEGF/PDGF 通路对 CM VM 的抑制作用。免疫组化(IHC)证实了血管内皮生长因子(VEGF)和表皮生长因子(PDGF)表达升高的 CM 中的血管瘤。缺氧促进了 CM 的增殖,上调了 HIF-1α、VEGF 和 PDGF。VEGF 和 PDGF 增强了 CM 的迁移、侵袭和 VM,其中 HIF-1α 起着关键作用。ART通过抑制HIF-1α/VEGF/PDGF通路缓解了VM的形成,突出了其作为CM抗肿瘤药物的潜力。