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@ARTICLE{Teng:301501,
      author       = {Y.-H. Teng and B. Appiah and G. Andrieux and M. Schrempp
                      and K. Rose and A. S. Hofmann and M. Ku and S. Beyes and M.
                      Boerries$^*$ and A. Hecht},
      title        = {{TGF}-β signaling redirects {S}ox11 gene regulatory
                      activity to promote partial {EMT} and collective invasion of
                      oncogenically transformed intestinal organoids.},
      journal      = {Oncogenesis},
      volume       = {14},
      number       = {1},
      issn         = {2157-9024},
      address      = {[Erscheinungsort nicht ermittelbar]},
      publisher    = {Nature Publ.},
      reportid     = {DKFZ-2025-01040},
      pages        = {17},
      year         = {2025},
      abstract     = {Cancer cells infiltrating surrounding tissue frequently
                      undergo partial epithelial-mesenchymal transitions (pEMT)
                      and employ a collective mode of invasion. How these
                      phenotypic traits are regulated and interconnected remains
                      underexplored. Here, we used intestinal organoids with
                      colorectal cancer (CRC) driver mutations as model system to
                      investigate the mechanistic basis of TGF-β1-induced pEMT
                      and collective invasion. By scRNA-seq we identified multiple
                      cell subpopulations representing a broad pEMT spectrum,
                      where the most advanced pEMT state correlated with the
                      transcriptional profiles of leader cells in collective
                      invasion and a poor prognosis mesenchymal subtype of human
                      CRC. Bioinformatic analyses pinpointed Sox11 as a
                      transcription factor gene whose expression peaked in the
                      potential leader/pEMThigh cells. Immunofluorescence staining
                      confirmed Sox11 expression in cells at the invasive front of
                      TGF-β1-treated organoids. Loss-of-function and
                      overexpression experiments showed that Sox11 is necessary,
                      albeit not sufficient, for TGF-β1-induced pEMT and
                      collective invasion. In human CRC samples, elevated SOX11
                      expression was associated with advanced tumor stages and
                      worse prognosis. Unexpectedly, aside from orchestrating the
                      organoid response to TGF-β1, Sox11 controlled expression of
                      genes related to normal gut function and tumor suppression.
                      Apparently, Sox11 is embedded in several distinct gene
                      regulatory circuits, contributing to intestinal tissue
                      homeostasis, tumor suppression, and TGF-β-mediated cancer
                      cell invasion.},
      cin          = {FR01},
      ddc          = {610},
      cid          = {I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40393982},
      doi          = {10.1038/s41389-025-00560-7},
      url          = {https://inrepo02.dkfz.de/record/301501},
}