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@ARTICLE{Roh:144698,
      author       = {V. Roh and A. Hiou-Feige and V. Misetic and J.-P. Rivals
                      and J. Sponarova and M.-T. Teh and S. Ferreira Lopes and Z.
                      Truan and M. Mermod and Y. Monnier and J. Hess$^*$ and G. V.
                      Tolstonog and C. Simon},
      title        = {{T}he transcription factor {FOXM}1 regulates the balance
                      between proliferation and aberrant differentiation in head
                      and neck squamous cell carcinoma.},
      journal      = {The journal of pathology},
      volume       = {250},
      number       = {1},
      issn         = {1096-9896},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2019-02140},
      pages        = {107-119},
      year         = {2020},
      note         = {2020 Jan;250(1):107-119},
      abstract     = {Sustained expression of FOXM1 is a hallmark of nearly all
                      human cancers including squamous cell carcinomas of the head
                      and neck (HNSCC). HNSCCs partially preserve the epithelial
                      differentiation program, which recapitulates fetal and adult
                      traits of the tissue of tumor origin but is deregulated by
                      genetic alterations and tumor-supporting pathways. Using
                      shRNA-induced knockdown, we demonstrate a minimal impact of
                      FOXM1 on proliferation and migration of HNSCC cell lines
                      under standard cell culture conditions. However, FOXM1
                      knockdown in three-dimensional (3D) culture and xenograft
                      tumor models resulted in reduced proliferation, decreased
                      invasion and a more differentiated-like phenotype,
                      indicating a context dependent modulation of FOXM1 activity
                      in HNSCC cells. By ectopic overexpression of FOXM1 in HNSCC
                      cell lines, we demonstrate a reduced expression of
                      cutaneous-type keratin K1 and involucrin as a marker of
                      squamous differentiation, supporting the role of FOXM1 in
                      modulation of aberrant differentiation in HNSCC. Thus, our
                      data provide a strong rationale for targeting FOXM1 in
                      HNSCC. This article is protected by copyright. All rights
                      reserved.},
      cin          = {A102},
      ddc          = {610},
      cid          = {I:(DE-He78)A102-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31465124},
      doi          = {10.1002/path.5342},
      url          = {https://inrepo02.dkfz.de/record/144698},
}