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https://www.selleckchem.com/JAK.html Glycosylation plays an important role in the genesis of various cancers. The inhibition of glycosylation disturbs the protein folding machinery, causing the accumulation of unfolded proteins in the cell endoplasmic reticulum (ER) and inducing ER stress. Tunicamycin (TM) is an inhibitor of glycosylation that has shown marked antitumor activity. In this study, we investigated the effect of TM on the tumorigenesis of head and neck cancer cells. The effects of TM on cell proliferation, colony formation and tumorsphere formation in vitro and tumorigenicity in vivo were investigated in head and neck cancer cells. ER stress was determined by the evaluation of PERK, PDI, IRE1-α, BIP, Ero1-Lα and calnexin expression using western blotting and immunofluorescence. We found that TM inhibited colony formation and tumorsphere formation of head and neck cancer cells in vitro and suppressed tumor growth in vivo. After incubation with TM, the expression of the cancer stem cell markers CD44 and Bmi-1 was reduced, and the expression of the ER stress markers BIP, Ero1-Lα and calnexin was elevated. Moreover, the EGFR signaling pathway was inhibited, and nonglycosylated EGFR degradation was accelerated with TM treatment. Our results suggest that inhibition of glycosylation by TM may be a novel treatment strategy for use with HNSCC patients. AJTR Copyright © 2020.AIMS In previous studies, numerous differential lncRNAs were identified via RNA-sequencing. In this dysregulated lncRNAs, lincRNA02471 attracted our attention due to its highest fold change. The aims of our study mainly focused on the function and mechanism of lincRNA02471 in papillary thyroid cancer. MATERIALS AND METHODS Overexpression and knockdown vectors were constructed to investigate the function of lincRNA02471. Proliferation, apoptosis, invasion and EMT were performed to assess the function of lincRNA02471. Dual-luciferase reporter assay was performed to explore the relationship betwe

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