% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Klose:128912,
      author       = {J. Klose and J. Eissele and C. Volz and S. Schmitt$^*$ and
                      A. Ritter and S. Ying and T. Schmidt and U. Heger and M.
                      Schneider and A. Ulrich},
      title        = {{S}alinomycin inhibits metastatic colorectal cancer growth
                      and interferes with {W}nt/β-catenin signaling in {CD}133(+)
                      human colorectal cancer cells.},
      journal      = {BMC cancer},
      volume       = {16},
      number       = {1},
      issn         = {1471-2407},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DKFZ-2017-04925},
      pages        = {896},
      year         = {2016},
      abstract     = {The polyether antibiotic Salinomycin (Sal) is regarded as
                      an inhibitor of cancer stem cells. Its effectiveness on
                      human colorectal cancer (CRC) cells in vitro has been
                      demonstrated before. The aim of this study was to establish
                      a murine model to investigate the effectiveness of Sal in
                      vivo. Furthermore, we investigated the impact of Sal on
                      Wnt/β-catenin signaling in human CD133(+) CRC cells.The two
                      murine CRC cell lines MC38 and CT26 were used to analyze the
                      impact of Sal on tumor cell proliferation, viability,
                      migration, cell cycle progression and cell death in vitro.
                      For in vivo studies, CT26 cells were injected into syngeneic
                      BALB/c mice to initiate (i) subcutaneous, (ii) orthotopic,
                      or (iii) metastatic CRC growth. Sal was administered daily,
                      5-Fluoruracil served as a control. For mechanistic studies,
                      the CD133(+)and CD133(-) subpopulations of human CRC cells
                      were separated by flow cytometry and separately exposed to
                      increasing concentrations of Sal. The impact on
                      Wnt/β-catenin signaling was determined by Western blotting
                      and quantitative PCR.Sal markedly impaired tumor cell
                      viability, proliferation and migration, and induced necrotic
                      cell death in vitro. CRC growth in vivo was likewise
                      inhibited upon Sal treatment. Interference with Wnt
                      signaling and reduced expression of the Wnt target genes
                      Fibronectin and Lgr5 indicates a novel molecular mechanism,
                      mediating anti-tumoral effects of Sal in CRC.Sal effectively
                      impairs CRC growth in vivo. Furthermore, Sal acts as an
                      inhibitor of Wnt/β-catenin signaling. Thus, Salinomycin
                      represents a promising candidate for clinical CRC
                      treatment.},
      keywords     = {AC133 Antigen (NLM Chemicals) / PROM1 protein, human (NLM
                      Chemicals) / Pyrans (NLM Chemicals) / salinomycin (NLM
                      Chemicals)},
      cin          = {W220},
      ddc          = {610},
      cid          = {I:(DE-He78)W220-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27855654},
      pmc          = {pmc:PMC5114842},
      doi          = {10.1186/s12885-016-2879-8},
      url          = {https://inrepo02.dkfz.de/record/128912},
}