Tunicamycin induces ER stress and inhibits tumorigenesis of head and neck cancer cells by inhibiting N-glycosylation.
Yang Wang, Ling Zhang, Zhiyan He, Jiong Deng, Zhiyuan Zhang, Liu Liu, Weimin Ye, Shuli Liu
Abstract
. 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.
Topics & Concepts
TunicamycinUnfolded protein responseCalnexinEndoplasmic reticulumGlycosylationCancer researchCarcinogenesisIn vivoCancer cellCell growthChemistryCell biologyBiologyCancerCalreticulinMedicineInternal medicineBiochemistryBiotechnologyGlycosylation and Glycoproteins ResearchGalectins and Cancer BiologyUbiquitin and proteasome pathways