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Paul, Mariel C.; Schneeweis, Christian; Falcomatà, Chiara; Shan, Chuan; Rossmeisl, Daniel; Koutsouli, Stella; Klement, Christine; Zukowska, Magdalena; Widholz, Sebastian A.; Jesinghaus, Moritz; Heuermann, Konstanze K.; Engleitner, Thomas; Seidler, Barbara; Sleiman, Katia; Steiger, Katja; Tschurtschenthaler, Markus; Walter, Benjamin; Weidemann, Sören A.; Pietsch, Regina; Schnieke, Angelika; Schmid, Roland M.; Robles, Maria S.; Andrieux, Geoffroy; Boerries, Melanie; [...]

Non-canonical functions of SNAIL drive context-specific cancer progression

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  • Medientyp: E-Artikel
  • Titel: Non-canonical functions of SNAIL drive context-specific cancer progression
  • Beteiligte: Paul, Mariel C.; Schneeweis, Christian; Falcomatà, Chiara; Shan, Chuan; Rossmeisl, Daniel; Koutsouli, Stella; Klement, Christine; Zukowska, Magdalena; Widholz, Sebastian A.; Jesinghaus, Moritz; Heuermann, Konstanze K.; Engleitner, Thomas; Seidler, Barbara; Sleiman, Katia; Steiger, Katja; Tschurtschenthaler, Markus; Walter, Benjamin; Weidemann, Sören A.; Pietsch, Regina; Schnieke, Angelika; Schmid, Roland M.; Robles, Maria S.; Andrieux, Geoffroy; Boerries, Melanie; [...]
  • Erschienen: Springer Science and Business Media LLC, 2023
  • Erschienen in: Nature Communications
  • Sprache: Englisch
  • DOI: 10.1038/s41467-023-36505-0
  • ISSN: 2041-1723
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:title>Abstract</jats:title><jats:p>SNAIL is a key transcriptional regulator in embryonic development and cancer. Its effects in physiology and disease are believed to be linked to its role as a master regulator of epithelial-to-mesenchymal transition (EMT). Here, we report EMT-independent oncogenic SNAIL functions in cancer. Using genetic models, we systematically interrogated SNAIL effects in various oncogenic backgrounds and tissue types. SNAIL-related phenotypes displayed remarkable tissue- and genetic context-dependencies, ranging from protective effects as observed in KRAS- or WNT-driven intestinal cancers, to dramatic acceleration of tumorigenesis, as shown in KRAS-induced pancreatic cancer. Unexpectedly, SNAIL-driven oncogenesis was not associated with E-cadherin downregulation or induction of an overt EMT program. Instead, we show that SNAIL induces bypass of senescence and cell cycle progression through p16<jats:sup>INK4A</jats:sup>-independent inactivation of the Retinoblastoma (RB)-restriction checkpoint. Collectively, our work identifies non-canonical EMT-independent functions of SNAIL and unravel its complex context-dependent role in cancer.</jats:p>
  • Zugangsstatus: Freier Zugang