Treatment with FK228 alters expression of enzymes in the biosynthetic pathways for a large number of glycome related genes including enzymes in all major glycosylation pathways and several glycan binding proteins. Differential sensitivity to paclitaxel, proliferation, and MMP activity were also assessed. Differential glycosylation was then assessed by lectin binding arrays and the ability of cellular proteins to bind to glycans was assessed by glycan binding arrays. In comparing HDAC inhibitor treated and control cells, differential expression of glycome-related genes were assessed by microarray. MethodsĮpigenetically plastic SW13 adrenocortical carcinoma cells were treated with FK228, an HDAC inhibitor with high affinity for HDAC1 and, to a lesser extent, HDAC2. This study focuses on the ability of HDAC inhibition to alter glycosylation and to lead to pro-oncogenic alterations in the glycome as assessed by metastatic potential and chemoresistance. Although the type of glycosylation is determined by protein sequence encoded by the genome, the extent and modifications of glycosylation depends on the activity of biosynthetic enzymes and recent data suggests that the glycome is also subject to epigenetic regulation. ANSI Compliant.Ĭertified RNase, DNase, PCR Inhibitors, and human DNA Free.Defects in the type and degree of cellular glycosylation impact oncogenesis on multiple levels. Not for use in diagnostic procedures.Ĭertified RNase and DNase Free. ANSI Compliantĩ6-well Polypropylene Sample Processing & Storage PlatesĪLPS5000, ALPS3000, and ALPS50V Heat Sealers, Automated Liquid Handlers, Multidrop Combi, Centrifuges, Ultralow Freezers, Liquid HandlersĪutomation Liquid Handlers, Biobanking, Genomics, Sample Prep, NGS, Sequencing, Long and Short Term Storage, Drug Discovery, Vaccine Research, PCR and qPCR sample preparationįor Research Use Only. Certified RNase, DNase, PCR Inhibitors, and human DNA Free.
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