Tunicamycin is a mixture of homologous nucleoside antibiotics. An inhibitor of glycosylation. Tunicamycin Blocks the formation of N-glycosidic linkages by inhibiting the first step in glycoprotein synthesis. In vitro: Tunicamycin causes accumulation of unfolded proteins in cell endoplasmic reticulum (ER). Tunicamycin-induced ER stress suppresses CD44+/CD24- phenotype cell subpopulation. Tunicamycin inhibite invasion, increase cell death, suppress proliferation and reduce migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture. [1] In vivo: Administering tunicamycin further increase protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVALPS-OVA mice. [2]

• [1]. Nami B et al. Tunicamycin-induced endoplasmic reticulum stress reduces in vitro subpopulation and invasion of CD44+/CD24- phenotype breast cancer stem cells. Exp Toxicol Pathol. 2016 Aug;68(7):419-26.

  [2]. Guo Q et al. Tunicamycin Aggravates Endoplasmic Reticulum Stress and Airway Inflammation via PERK-ATF4-CHOP Signaling in a Murine Model of Neutrophilic Asthma. J Asthma. 2016 Jul 6