Alterations in the glycome after HDAC inhibition impact oncogenic potential in epigenetically plastic SW13 cells

摘要: Defects in the type and degree of cellular glycosylation impact oncogenesis on multiple levels. Although is determined by protein sequence encoded genome, extent modifications depends activity biosynthetic enzymes recent data suggests that glycome also subject to epigenetic regulation. This study focuses ability HDAC inhibition alter lead pro-oncogenic alterations as assessed metastatic potential chemoresistance. Epigenetically plastic SW13 adrenocortical carcinoma cells were treated with FK228, an inhibitor high affinity for HDAC1 and, a lesser extent, HDAC2. In comparing control cells, differential expression glycome-related genes microarray. Differential was then lectin binding arrays proteins bind glycans glycan arrays. sensitivity paclitaxel, proliferation, MMP assessed. Treatment FK228 alters pathways large number related including all major several proteins. 84% these differentially expressed are linked cancer, some prognostic markers others contributing basic oncogenic functions such metastasis or Glycan appear be extracts from untreated show The mRNA documented binding. However, assessment changes complicated fact detection through dependent methods used prepare samples protein-rich lysates different than fixed cases. Paralleling glycome, treatment increases reduces paclitaxel. substantially altered may have far-reaching impacts oncogenesis.