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@ARTICLE{Schwarzmueller:294580,
      author       = {L. J. Schwarzmueller and R. S. Adam and L. F. Moreno and L.
                      E. Nijman and A. Logiantara and S. Eleonora and O. Bril and
                      S. Vromans and N. E. de Groot and F. P. Giugliano and E.
                      Stepanova$^*$ and V. Muncan and C. C. Elbers and K. J. Lenos
                      and D. A. Zwijnenburg and M. A. J. van Eijndhoven and D. M.
                      Pegtel and S. M. van Neerven and F. Loayza-Puch$^*$ and T.
                      Dadali and W. J. Broom and M. A. Maier and J. Koster and L.
                      Vermeulen and N. Léveillé},
      title        = {{I}dentifying colorectal cancer-specific vulnerabilities in
                      the {W}nt-driven long non-coding transcriptome.},
      journal      = {Gut},
      volume       = {74},
      number       = {4},
      issn         = {0017-5749},
      address      = {London},
      publisher    = {BMJ Publishing Group},
      reportid     = {DKFZ-2024-02355},
      pages        = {571-585},
      year         = {2025},
      note         = {2025 Mar 6;74(4):571-585},
      abstract     = {Aberrant Wnt pathway activation is a key driver of
                      colorectal cancer (CRC) and is essential to sustain tumour
                      growth and progression. Although the downstream
                      protein-coding target genes of the Wnt cascade are well
                      known, the long non-coding transcriptome has not yet been
                      fully resolved.In this study, we aim to comprehensively
                      reveal the Wnt-regulated long non-coding transcriptome and
                      exploit essential molecules as novel therapeutic targets.We
                      used global run-on sequencing to define β-catenin-regulated
                      long non-coding RNAs (lncRNAs) in CRC. CRISPRi dropout
                      screens were subsequently used to establish the functional
                      relevance of a subset of these lncRNAs for long-term
                      expansion of CRC.We uncovered that LINC02418 is essential
                      for cancer cell clonogenic outgrowth. Mechanistically,
                      LINC02418 regulates MYC expression levels to promote CRC
                      stem cell functionality and prevent terminal
                      differentiation. Furthermore, we developed effective small
                      interfering RNA (siRNA)-based therapeutics to target
                      LINC02418 RNA in vivo.We propose that cancer-specific
                      Wnt-regulated lncRNAs provide novel therapeutic
                      opportunities to interfere with the Wnt pathway, which has
                      so far defied effective pharmacological inhibition.},
      keywords     = {colorectal cancer (Other)},
      cin          = {B250},
      ddc          = {610},
      cid          = {I:(DE-He78)B250-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39562049},
      doi          = {10.1136/gutjnl-2024-332752},
      url          = {https://inrepo02.dkfz.de/record/294580},
}