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@ARTICLE{Fritzsche:309695,
      author       = {S. Fritzsche and R. N. Sugiyanto and K. Gür and A. Krumme
                      and M. L. Marois and A. Fraas and A. Inal and M. Huerta and
                      V. Henriques and E. Eiteneuer and T. Albrecht and A. Charbel
                      and M. T. Dill$^*$ and C. Sticht and C. De La Torre and S.
                      Pusch and A. Mehrabi and K. Breuhahn and J. Ji and P.
                      Schirmacher and B. Goeppert and S. Roessler$^*$},
      title        = {{S}trawberry {N}otch 1 {A}cts as a {T}ranscriptional
                      {R}egulator {D}riving {O}ncogenic {P}rograms in {L}iver
                      {C}arcinogenesis.},
      journal      = {Advanced science},
      volume       = {nn},
      issn         = {2198-3844},
      address      = {Weinheim},
      publisher    = {Wiley-VCH},
      reportid     = {DKFZ-2026-00308},
      pages        = {nn},
      year         = {2026},
      note         = {#DKTKZFB9# / epub},
      abstract     = {Aberrant Notch signaling has been identified as a key
                      driver of cancer development. Genetic studies in Drosophila
                      showed that the knockout of strawberry notch (sno) mimics
                      the loss of notch. Here, we found that Strawberry Notch 1
                      (SBNO1) is upregulated in several cancer entities and
                      elucidated the role of SBNO1 in liver cancer development. In
                      hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA),
                      SBNO1 protein was significantly increased and localized to
                      the nucleus suggesting its involvement in gene regulation.
                      SBNO1-inhibition reduced cell viability, colony formation
                      and migration and induced distinct expression patterns in
                      HCC and CCA cell lines. However, BioID revealed that SBNO1
                      similarly modulates gene regulation in HCC and CCA by
                      binding to general transcription factors TAF4 and TAF3.
                      Deletion of Sbno1 in murine liver cancer cells Hep55.1C
                      reduced tumor growth in vivo. In addition, inhibition of
                      Sbno1 significantly reduced liver tumor development in three
                      different mouse models of HCC and CCA. Furthermore,
                      Sbno1-deletion reduced biliary differentiation and
                      angiogenesis in the tumor margin, underscoring the necessity
                      of Sbno1 in Notch-driven CCA formation. Thus, we identified
                      SBNO1 as a transcriptional regulator required for liver
                      cancer development and progression.},
      keywords     = {SBNO1 (Other) / cancer (Other) / cholangiocarcinoma (Other)
                      / hepatocellular carcinoma (Other) / notch signaling
                      (Other)},
      cin          = {D500 / HD01},
      ddc          = {624},
      cid          = {I:(DE-He78)D500-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41649174},
      doi          = {10.1002/advs.202507238},
      url          = {https://inrepo02.dkfz.de/record/309695},
}