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Oridonin enhances TRAIL-induced apoptosis through GALNT14-mediated DR5 glycosylation.

Abstract
Oridonin is a diterpenoid isolated from the Rabdosia rubescens and has multiple biological effects, such as anti-inflammation and anti-tumor activities. In present study, we revealed that the sensitizing effect of oridonin on tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in several cancer cells, but not in normal cells. Oridonin enhanced death-signaling inducing complexes (DISC) formation and DR5 glycosylation without affecting expression of downstream intracellular apoptosis-related proteins. Oridonin upregulated peptidyl O-glycosyltransferase GALNT14 in a dose- and time-dependent manner. Knockdown of GALNT14 by siRNA and Endo H treatment reduced oridonin-induced DR5 glycosylation. Furthermore, treatment with inhibitor of glycosylation (benzyl-α-GalNAc) blocked oridonin plus TRAIL-induced apoptosis. Collectively, our results suggest that oridonin-induced DR5 glycosylation contributes to TRAIL-induced apoptotic cell death in cancer cells.
AuthorsMi-Yeon Jeon, Seung Un Seo, Seon Min Woo, Kyoung-Jin Min, Hee Sun Byun, Gang Min Hur, Sun Chul Kang, Taeg Kyu Kwon
JournalBiochimie (Biochimie) Vol. 165 Pg. 108-114 (Oct 2019) ISSN: 1638-6183 [Electronic] France
PMID31336136 (Publication Type: Journal Article)
CopyrightCopyright © 2019 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM). All rights reserved.
Chemical References
  • Apoptosis Regulatory Proteins
  • Diterpenes, Kaurane
  • Receptors, TNF-Related Apoptosis-Inducing Ligand
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFRSF10B protein, human
  • oridonin
  • N-Acetylgalactosaminyltransferases
  • UDP-N-acetyl-D-galactosamine polypeptide N-acetylgalactosaminyltransferase 14, human
Topics
  • Apoptosis (drug effects)
  • Apoptosis Regulatory Proteins (metabolism)
  • Cell Line
  • Diterpenes, Kaurane (pharmacology)
  • Glycosylation
  • Humans
  • N-Acetylgalactosaminyltransferases (metabolism)
  • Receptors, TNF-Related Apoptosis-Inducing Ligand (metabolism)
  • TNF-Related Apoptosis-Inducing Ligand (pharmacology, physiology)

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