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@ARTICLE{Schrader:127482,
      author       = {C. H. Schrader$^*$ and M. Kolb and K. Zaoui and C.
                      Flechtenmacher and N. Grabe$^*$ and K.-J. Weber and T.
                      Hielscher$^*$ and P. K. Plinkert and J. Hess$^*$},
      title        = {{K}allikrein-related peptidase 6 regulates
                      epithelial-to-mesenchymal transition and serves as
                      prognostic biomarker for head and neck squamous cell
                      carcinoma patients.},
      journal      = {Molecular cancer},
      volume       = {14},
      number       = {1},
      issn         = {1476-4598},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DKFZ-2017-03505},
      pages        = {107},
      year         = {2015},
      abstract     = {Dysregulated expression of Kallikrein-related peptidase 6
                      (KLK6) is a common feature for many human malignancies and
                      numerous studies evaluated KLK6 as a promising biomarker for
                      early diagnosis or unfavorable prognosis. However, the
                      expression of KLK6 in carcinomas derived from mucosal
                      epithelia, including head and neck squamous cell carcinoma
                      (HNSCC), and its mode of action has not been addressed so
                      far.Stable clones of human mucosal tumor cell lines were
                      generated with shRNA-mediated silencing or ectopic
                      overexpression to characterize the impact of KLK6 on tumor
                      relevant processes in vitro. Tissue microarrays with primary
                      HNSCC samples from a retrospective patient cohort
                      (n = 162) were stained by immunohistochemistry and the
                      correlation between KLK6 staining and survival was addressed
                      by univariate Kaplan-Meier and multivariate Cox proportional
                      hazard model analysis.KLK6 expression was detected in head
                      and neck tumor cell lines (FaDu, Cal27 and SCC25), but not
                      in HeLa cervix carcinoma cells. Silencing in FaDu cells and
                      ectopic expression in HeLa cells unraveled an inhibitory
                      function of KLK6 on tumor cell proliferation and mobility.
                      FaDu clones with silenced KLK6 expression displayed
                      molecular features resembling epithelial-to-mesenchymal
                      transition, nuclear β-catenin accumulation and higher
                      resistance against irradiation. Low KLK6 protein expression
                      in primary tumors from oropharyngeal and laryngeal SCC
                      patients was significantly correlated with poor
                      progression-free (p = 0.001) and overall survival
                      (p < 0.0005), and served as an independent risk factor
                      for unfavorable clinical outcome.In summary, detection of
                      low KLK6 expression in primary tumors represents a promising
                      tool to stratify HNSCC patients with high risk for treatment
                      failure. These patients might benefit from restoration of
                      KLK6 expression or pharmacological targeting of signaling
                      pathways implicated in EMT.},
      keywords     = {Biomarkers, Tumor (NLM Chemicals) / beta Catenin (NLM
                      Chemicals) / KLK6 protein, human (NLM Chemicals) /
                      Kallikreins (NLM Chemicals)},
      cin          = {C060 / G405 / V964 / D120},
      ddc          = {610},
      cid          = {I:(DE-He78)C060-20160331 / I:(DE-He78)G405-20160331 /
                      I:(DE-He78)V964-20160331 / I:(DE-He78)D120-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25990935},
      pmc          = {pmc:PMC4437453},
      doi          = {10.1186/s12943-015-0381-6},
      url          = {https://inrepo02.dkfz.de/record/127482},
}