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@ARTICLE{Yang:127817,
      author       = {C. Yang$^*$ and R. Fischer-Kešo$^*$ and T. Schlechter$^*$
                      and P. Ströbel and A. Marx and I. Hofmann$^*$},
      title        = {{P}lakophilin 1-deficient cells upregulate {SPOCK}1:
                      implications for prostate cancer progression.},
      journal      = {Tumor biology},
      volume       = {36},
      number       = {12},
      issn         = {1423-0380},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {DKFZ-2017-03839},
      pages        = {9567 - 9577},
      year         = {2015},
      abstract     = {Plakophilin (PKP) 1 is frequently downregulated in prostate
                      cancer and therefore may play a tumor-suppressive role. In
                      the present study, we stably knocked down PKP1 in the
                      non-neoplastic, prostatic BPH-1 cell line. In the
                      PKP1-deficient cells, the expression of keratin 14 was lost,
                      and the apoptosis rate was significantly reduced indicating
                      that the cells acquired new biological capabilities.
                      Moreover, we analyzed the gene expression profile of the
                      PKP1-deficient BPH-1 cells. Among the genes that were
                      significantly altered upon PKP1 knockdown, we noticed
                      several extracellular matrix (ECM)-related genes and
                      identified sparc/osteonectin, cwcv, and kazal-like domains
                      proteoglycan 1 (SPOCK1/testican-1) as a gene of interest.
                      SPOCK1 is a component of the ECM and belongs to a
                      matricellular protein family named secreted protein, acidic,
                      cysteine-rich (SPARC). The role of SPOCK1 in prostate cancer
                      has not been clearly elucidated. We analyzed SPOCK1 mRNA
                      expression levels in different cancer databases and
                      characterized its expression in 136 prostatic
                      adenocarcinomas by immunohistochemistry and western blot.
                      SPOCK1 revealed a cytoplasmic localization in the glandular
                      epithelium of the prostate and showed a significant
                      upregulation of mRNA and protein in prostate tumor samples.
                      Our findings support the hypothesis that PKP1 may have a
                      tumor-suppressive function and suggest an important role of
                      SPOCK1 in prostate tumor progression. Collectively, altered
                      expression of PKP1 and SPOCK1 appears to be a frequent and
                      critical event in prostate cancer.},
      keywords     = {PKP1 protein, human (NLM Chemicals) / Plakophilins (NLM
                      Chemicals) / Proteoglycans (NLM Chemicals) / RNA, Messenger
                      (NLM Chemicals) / SPOCK1 protein, human (NLM Chemicals)},
      cin          = {A190},
      ddc          = {570},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26138584},
      doi          = {10.1007/s13277-015-3628-3},
      url          = {https://inrepo02.dkfz.de/record/127817},
}