• Medientyp: E-Artikel
  • Titel: Immature truncated O-glycophenotype of cancer directly induces oncogenic features
  • Beteiligte: Radhakrishnan, Prakash; Dabelsteen, Sally; Madsen, Frey Brus; Francavilla, Chiara; Kopp, Katharina L.; Steentoft, Catharina; Vakhrushev, Sergey Y.; Olsen, Jesper V.; Hansen, Lars; Bennett, Eric P.; Woetmann, Anders; Yin, Guangliang; Chen, Longyun; Song, Haiyan; Bak, Mads; Hlady, Ryan A.; Peters, Staci L.; Opavsky, Rene; Thode, Christenze; Qvortrup, Klaus; Schjoldager, Katrine T.-B. G.; Clausen, Henrik; Hollingsworth, Michael A.; Wandall, Hans H.
  • Erschienen: Proceedings of the National Academy of Sciences, 2014
  • Erschienen in: Proceedings of the National Academy of Sciences
  • Sprache: Englisch
  • DOI: 10.1073/pnas.1406619111
  • ISSN: 0027-8424; 1091-6490
  • Schlagwörter: Multidisciplinary
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:title>Significance</jats:title> <jats:p> Cancer cells characteristically express proteins with immature O-glycosylation, but how and why cancer cells express immature O-glycans has remained poorly understood. Here, we report that one prevalent mechanism in pancreatic cancer is epigenetic silencing, rather than somatic mutations in a key chaperone, core 1 β3-Gal-T-specific molecular chaperone ( <jats:italic>COSMC</jats:italic> ), required for mature elongated O-glycosylation. We also demonstrate, with the use of well-defined cell systems generated by precise gene editing, that the aberrant O-glycophenotype by itself induces oncogenic features with enhanced growth and invasion. Our study suggests that the characteristic aberrant O-glycophenotype is critical for the development and behavior of cancer and further provides support for immunotherapeutic strategies that target aberrant O-glycans. </jats:p>
  • Zugangsstatus: Freier Zugang