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@ARTICLE{Dong:275927,
      author       = {H. Dong and L. Zeng and W. Chen and Q. Zhang and F. Wang
                      and Y. Wu and B. Cui and J. Qi and X. Zhang and C. Liu and
                      J. Deng and Y. Yu and C. A. Schmitt$^*$ and J. Du},
      title        = {{N}6-methyladenine-mediated aberrant activation of the
                      lnc{RNA} {SOX}2{OT}-{GLI}1 loop promotes non-small-cell lung
                      cancer stemness.},
      journal      = {Cell death discovery},
      volume       = {9},
      number       = {1},
      issn         = {2058-7716},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2023-00915},
      pages        = {149},
      year         = {2023},
      abstract     = {Despite the advent of precision medicine and immunotherapy,
                      mortality due to lung cancer remains high. The sonic
                      hedgehog (SHH) cascade and its key terminal factor,
                      glioma-associated oncogene homolog 1 (GLI1), play a pivotal
                      role in the stemness and drug resistance of lung cancer.
                      Here, we investigated the molecular mechanism of
                      non-canonical aberrant GLI1 upregulation. The SHH cascade
                      was upregulated in stem spheres and chemo-resistant lung
                      cancer cells and was accountable for drug resistance against
                      multiple chemotherapy regimens. GLI1 and the long non-coding
                      RNA SOX2OT were positively regulated, and the GLI1-SOX2OT
                      loop mediated the proliferation of parental and stem-like
                      lung cancer cells. Further mechanistic investigation
                      revealed that SOX2OT facilitated METTL3/14/IGF2BP2-mediated
                      m6A modification and stabilization of the GLI1 mRNA.
                      Additionally, SOX2OT upregulated METTL3/14/IGF2BP2 by
                      sponging miR-186-5p. Functional analysis corroborated that
                      GLI1 acted as a downstream target of METTL3/14/IGF2BP2, and
                      GLI1 silencing could block the oncogenicity of lung cancer
                      stem-like cells. Pharmacological inhibition of the loop
                      remarkably inhibited the oncogenesis of lung cancer cells in
                      vivo. Compared with paired adjacent normal tissues, lung
                      cancer specimens exhibited consistently upregulated
                      GLI1/SOX2OT/METTL3/14/IGF2BP2. The m6A-modified GLI1-SOX2OT
                      loop may serve as a potential therapeutic target and
                      prognostic predictor for lung cancer therapy and diagnosis
                      in the clinic.},
      cin          = {BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37149646},
      pmc          = {pmc:PMC10164154},
      doi          = {10.1038/s41420-023-01442-w},
      url          = {https://inrepo02.dkfz.de/record/275927},
}