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FOXD2-AS1 silencing inhibited HNSCC cell migration and invasion, also affected the expression of epithelial-mesenchymal transition-related particles. ConclusionFOXD2-AS1 was a prognostic marker in customers with HNSCC and may even be a favorable novel therapy target for HNSCC.Aim To determine the effectation of the food-borne mycotoxin, fusaric acid (FA) on miR-200a, SUV39H1-mediated H3K9me3, genome stability and apoptosis in human liver (HepG2) cells and C57BL/6 mice livers. Products
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