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@ARTICLE{Xu:296083,
      author       = {J. Xu$^*$ and J. Koch$^*$ and C. Schmidt$^*$ and M.
                      Nientiedt and M. Neuberger and P. Erben and M. S. Michel and
                      M. Rodríguez-Paredes$^*$ and F. Lyko$^*$},
      title        = {{L}oss of {YTHDC}1 m6{A} reading function promotes
                      invasiveness in urothelial carcinoma of the bladder.},
      journal      = {Experimental $\&$ molecular medicine},
      volume       = {57},
      number       = {1},
      issn         = {1226-3613},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2025-00031},
      pages        = {118-130},
      year         = {2025},
      note         = {DKFZ-ZMBH Alliance / #EA:A130#LA:A130# / 2025
                      Feb;57(1):118-130},
      abstract     = {Bladder cancer poses significant clinical challenges due to
                      its high metastatic potential and poor prognosis, especially
                      when it progresses to muscle-invasive stages. Here, we show
                      that the m6A reader YTHDC1 is downregulated in
                      muscle-invasive bladder cancer and is negatively correlated
                      with the expression of epithelial‒mesenchymal transition
                      genes. The functional inhibition or depletion of YTHDC1
                      increased the migration and invasion of urothelial cells.
                      Integrative analysis of multimodal sequencing datasets
                      provided detailed insights into the molecular mechanisms
                      mediating YTHDC1-dependent phenotypes and identified SMAD6
                      as a key transcript involved in the invasiveness of
                      urothelial carcinoma of the bladder. Notably, SMAD6 mRNA
                      colocalized less with YTHDC1 in tumoral tissues than in
                      paratumoral tissues, indicating disrupted binding during
                      cancer progression. Our findings establish YTHDC1-dependent
                      m6A reading as a critical epitranscriptomic mechanism
                      regulating bladder cancer invasiveness and provide a
                      paradigm for the epitranscriptomic deregulation of
                      cancer-associated networks.},
      cin          = {A130 / W210},
      ddc          = {540},
      cid          = {I:(DE-He78)A130-20160331 / I:(DE-He78)W210-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39741187},
      doi          = {10.1038/s12276-024-01377-x},
      url          = {https://inrepo02.dkfz.de/record/296083},
}