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@ARTICLE{Zuidhof:299504,
      author       = {H. R. Zuidhof and C. Müller and G. Kortman and R.
                      Wardenaar and E. Stepanova$^*$ and F. Loayza-Puch$^*$ and C.
                      F. Calkhoven},
      title        = {{T}he m6{A} demethylase {FTO} promotes {C}/{EBP}β-{LIP}
                      translation to perform oncogenic functions in breast cancer
                      cells.},
      journal      = {The FEBS journal},
      volume       = {292},
      number       = {10},
      issn         = {0014-2956},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2025-00462},
      pages        = {2688-2709},
      year         = {2025},
      note         = {2025 May;292(10):2688-2709},
      abstract     = {N6-methyladenosine (m6A) is a prevalent posttranscriptional
                      mRNA modification involved in the regulation of transcript
                      turnover, translation, and other aspects of RNA fate. The
                      modification is mediated by multicomponent methyltransferase
                      complexes (so-called writers) and is reversed through the
                      action of the m6A-demethylases fat mass and
                      obesity-associated (FTO) and alkB homolog 5 (ALKBH5)
                      (so-called erasers). FTO promotes cell proliferation, colony
                      formation and metastasis in models of triple-negative breast
                      cancer (TNBC). However, little is known about genome-wide or
                      specific downstream regulation by FTO. Here, we examined
                      changes in the genome-wide transcriptome and translatome
                      following FTO knockdown in TNBC cells. Unexpectedly, FTO
                      knockdown had a limited effect on the translatome, while
                      transcriptome analysis revealed that genes related to
                      extracellular matrix (ECM) and epithelial-mesenchymal
                      transition (EMT) are regulated through yet unidentified
                      mechanisms. Differential translation of CEBPB mRNA into the
                      C/EBPβ transcription factor isoform C/EBPβ-LIP is known to
                      act in a pro-oncogenic manner in TNBC cells through
                      regulation of EMT genes. Here we show that FTO is required
                      for efficient C/EBPβ-LIP expression, suggesting that FTO
                      has oncogenic functions through regulation of C/EBPβ-LIP.},
      keywords     = {C/EBPβ (Other) / FTO (Other) / breast cancer (Other) /
                      mRNA translation (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:40022434},
      doi          = {DOI:10.1111/febs.70033},
      url          = {https://inrepo02.dkfz.de/record/299504},
}