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@ARTICLE{Schlensog:826699,
      author       = {Schlensog, Martin and Magnus, Lara and Heide, Timon and
                      Eschenbruch, Julian and Steib, Florian and Tator, Maximilian
                      and Kloten, Vera and Rose, Michael and Noetzel, Erik and
                      Gaisa, Nadine T. and Knüchel, Ruth and Dahl, Edgar},
      title        = {{E}pigenetic loss of putative tumor suppressor {SFRP}3
                      correlates with poor prognosis of lung adenocarcinoma
                      patients},
      journal      = {Epigenetics},
      volume       = {13},
      number       = {3},
      issn         = {1559-2308},
      address      = {Austin, Tex.},
      publisher    = {Landes Bioscience},
      reportid     = {FZJ-2017-00917},
      pages        = {214-227},
      year         = {2018},
      abstract     = {Secreted frizzled related protein 3 (SFRP3) contains a
                      cysteine-rich domain (CRD) that shares homology with
                      Frizzled CRD and regulates WNT signaling. Independent
                      studies showed epigenetic silencing of SFRP3 in melanoma and
                      hepatocellular carcinoma. Moreover, a tumor suppressive
                      function of SFRP3 was shown in androgen-independent prostate
                      and gastric cancer cells. The current study is the first to
                      investigate SFRP3 expression and its potential clinical
                      impact on non-small cell lung carcinoma (NSCLC). WNT
                      signaling components present on NSCLC subtypes were
                      preliminary elucidated by expression data of The Cancer
                      Genome Atlas (TCGA). We identified a distinct expression
                      signature of relevant WNT signaling components that differ
                      between adenocarcinoma (LUAD) and squamous cell carcinoma
                      (LUSC). Of interest, canonical WNT signaling is predominant
                      in LUAD samples and non-canonical WNT signaling is
                      predominant in LUSC. In line, high SFRP3 expression resulted
                      in beneficial clinical outcome for LUAD but not for LUSC
                      patients. Furthermore, SFRP3 mRNA expression was
                      significantly decreased in NSCLC tissue compared to normal
                      lung samples. TCGA data verified the reduction of SFRP3 in
                      LUAD and LUSC patients. Moreover, DNA hypermethylation of
                      SFRP3 was evaluated in the TCGA methylation dataset
                      resulting in epigenetic inactivation of SFRP3 expression in
                      LUAD, but not in LUSC, and was validated by pyrosequencing
                      of our NSCLC tissue cohort and in vitro demethylation
                      experiments. Immunohistochemistry confirmed SFRP3 protein
                      downregulation in primary NSCLC and indicated ...},
      cin          = {ICS-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-7-20110106},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27623992},
      UT           = {WOS:000434326600002},
      doi          = {10.1080/15592294.2016.1229730},
      url          = {https://juser.fz-juelich.de/record/826699},
}