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@ARTICLE{Paul:274160,
      author       = {M. C. Paul$^*$ and C. Schneeweis$^*$ and C. Falcomatà$^*$
                      and C. Shan$^*$ and D. Rossmeisl$^*$ and S. Koutsouli and C.
                      Klement$^*$ and M. Zukowska$^*$ and S. Widholz$^*$ and M.
                      Jesinghaus$^*$ and K. K. Heuermann$^*$ and T. Engleitner$^*$
                      and B. Seidler$^*$ and K. Sleiman$^*$ and K. Steiger and M.
                      Tschurtschenthaler$^*$ and B. Walter and S. A. Weidemann$^*$
                      and R. Pietsch$^*$ and A. Schnieke and R. M. Schmid and M.
                      S. Robles and G. Andrieux$^*$ and M. Börries$^*$ and R.
                      Rad$^*$ and G. Schneider$^*$ and D. K. M. Saur$^*$},
      title        = {{N}on-canonical functions of {SNAIL} drive context-specific
                      cancer progression.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-00462},
      pages        = {1201},
      year         = {2023},
      abstract     = {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 p16INK4A-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.},
      cin          = {MU01 / FR01},
      ddc          = {500},
      cid          = {I:(DE-He78)MU01-20160331 / I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36882420},
      doi          = {10.1038/s41467-023-36505-0},
      url          = {https://inrepo02.dkfz.de/record/274160},
}