Galectin-1 Promotes Vasculogenic Mimicry in Gastric Cancer by Upregulating EMT Signaling

摘要: Background: Galectin-1 (Gal-1) expression was positively associated with vasculogenic mimicry (VM) in primary gastric cancer (GC) tissue, and that both Gal-1 VM GC tissue are indicators of poor prognosis. However, whether promotes VM, by what mechanismsremains unknown. Methods: To investigate the underlying mechanisms,wound healing assay, proliferation invasion three-dimensional culture were used to evaluate invasion, metastasis promoted formation effects Gal-1. We monitored level sociated proteins tissues, cell lines vitro nude mice tumorigenicity vivo immunohistochemistry western blot. Results: overexpression significantly proliferation, migration, MGC-803 cells. E-cadherin vimentin clinical samples. The epithelial-to-mesenchymal transition (EMT) induced cells TGF-β1 accompanied activation promotion formation, while knockdown reduced response TGF-β1, suggesting activating EMT signaling. Overexpression accelerated subcutaneous xenograft growth facilitated pulmonary athymic mice, enhanced markers, vivo. Conclusion: Our results indicated upregulating signaling; thus, this pathway potential novel targets treat GC.