作者: Hongyan Han , Longsheng Du , Zhifei Cao , Bin Zhang , Quansheng Zhou
DOI: 10.1016/J.EJPHAR.2017.11.019
关键词: Promoter 、 VE-cadherin 、 Cancer research 、 CXCL2 、 Neovascularization 、 Chemistry 、 Chemokine 、 In vivo 、 Pancreatic cancer 、 Vasculogenic mimicry
摘要: Various aggressive cancers, including pancreatic cancer, produce functional blood vessels by neovascularization. Tumor vasculogenic mimicry (VM) promotes cancer progression and is closely associated with the poor prognosis of patients. Therefore, tumor VM a sensible target for novel anti-cancer drug discovery. However, there lack effective anti-tumor drugs in clinical setting. In this study, we aim to explore agents effectually inhibit cell-mediated therapy. Pancreatic cell lines Patu8988 Panc1 were utilized as model. A mouse model was used vitro capillary-like structure formation vivo Matrigel plug assays evaluate efficacy small molecule triptonide from traditional Chinese herbs. methods, RT-PCR, immunohistochemical staining, luciferase gene transcription reporter system, applied study mechanisms triptonide-exerted VM. Triptonide effectively inhibited cell-formed structures through suppressing migration, invasion, via inhibiting expression master VE-cadherin pro-migratory chemokine C-X-C motif ligand 2 (CXCL2), mainly reduction promoter activity. potently suppresses reducing migration invasion CXCL2 genes. Our results provide potent candidate further development anti-pancreatic