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@ARTICLE{Barbosa:287407,
      author       = {S. Barbosa$^*$ and N. K. Laureano$^*$ and W. W.
                      Hadiwikarta$^*$ and F. Visioli and M. Bonrouhi$^*$ and K.
                      Pajdzik and C. Conde-Lopez$^*$ and C. Herold-Mende and G.
                      Eidt$^*$ and R. Langie$^*$ and M. L. Lamers and F.
                      Stögbauer and J. Hess and I. Kurth$^*$ and A. Jou$^*$},
      title        = {{T}he {R}ole of {SOX}2 and {SOX}9 in {R}adioresistance and
                      {T}umor {R}ecurrence.},
      journal      = {Cancers},
      volume       = {16},
      number       = {2},
      issn         = {2072-6694},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2024-00222},
      pages        = {439},
      year         = {2024},
      note         = {#EA:E220#LA:E220#LA:E221#},
      abstract     = {Head and neck squamous cell carcinoma (HNSCC) exhibits
                      considerable variability in patient outcome. It has been
                      reported that SOX2 plays a role in proliferation, tumor
                      growth, drug resistance, and metastasis in a variety of
                      cancer types. Additionally, SOX9 has been implicated in
                      immune tolerance and treatment failures. SOX2 and SOX9
                      induce treatment failure by a molecular mechanism that has
                      not yet been elucidated. This study explores the inverse
                      association of SOX2/SOX9 and their distinct expression in
                      tumors, influencing the tumor microenvironment and
                      radiotherapy responses. Through public RNA sequencing data,
                      human biopsy samples, and knockdown cellular models, we
                      explored the effects of inverted SOX2 and SOX9 expression.
                      We found that patients expressing SOX2LowSOX9High showed
                      decreased survival compared to SOX2HighSOX9Low. A survival
                      analysis of patients stratified by radiotherapy and human
                      papillomavirus brings additional clinical relevance. We
                      identified a gene set signature comprising newly discovered
                      candidate genes resulting from inverted SOX2/SOX9
                      expression. Moreover, the TGF-β pathway emerges as a
                      significant predicted contributor to the overexpression of
                      these candidate genes. In vitro findings reveal that
                      silencing SOX2 enhances tumor radioresistance, while SOX9
                      silencing enhances radiosensitivity. These discoveries lay
                      the groundwork for further studies on the therapeutic
                      potential of transcription factors in optimizing HNSCC
                      treatment.},
      keywords     = {HNSCC (Other) / HPV negative (Other) / SOX2 (Other) / SOX9
                      (Other) / gene set signature (Other) / metastasis (Other) /
                      radiation treatment (Other)},
      cin          = {E220 / HD01 / E221},
      ddc          = {610},
      cid          = {I:(DE-He78)E220-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)E221-20160331},
      pnm          = {315 - Bildgebung und Radioonkologie (POF4-315)},
      pid          = {G:(DE-HGF)POF4-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38275880},
      pmc          = {pmc:PMC10814462},
      doi          = {10.3390/cancers16020439},
      url          = {https://inrepo02.dkfz.de/record/287407},
}