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@ARTICLE{Pervaiz:142993,
      author       = {A. Pervaiz$^*$ and M. Zepp$^*$ and S. Mahmood and D. M.
                      Ali$^*$ and M. Berger$^*$ and H. Adwan$^*$},
      title        = {{CCR}5 blockage by maraviroc: a potential therapeutic
                      option for metastatic breast cancer.},
      journal      = {Cellular oncology},
      volume       = {42},
      number       = {1},
      issn         = {2211-3436},
      address      = {Heidelberg [u.a.]},
      publisher    = {Springer},
      reportid     = {DKFZ-2019-00618},
      pages        = {93 - 106},
      year         = {2019},
      abstract     = {Bone metastasis is observed in up to $70\%$ of breast
                      cancer patients. The currently available treatment options
                      are palliative in nature. Chemokine receptor 5 (CCR5) has
                      gained attention as therapeutic target in various
                      malignancies. Here, we investigated the effects of targeting
                      CCR5 by its antagonist maraviroc in metastatic breast cancer
                      cells.In response to maraviroc exposure, cytotoxicity was
                      assessed using an MTT proliferation assay, whereas the
                      effects on colony formation and migration were assessed
                      using colony formation, transwell chamber migration and
                      scratch wound healing assays, respectively.
                      Apoptosis-related activities were investigated using nuclear
                      staining, annexin-V FITC staining and Western blotting. Cell
                      cycle changes were analysed using flow cytometry and qRT-PCR
                      for cell cycle relevant genes. A nude rat model for breast
                      cancer bone metastasis was used to evaluate the in vivo
                      efficacy of CCR5 targeting by maraviroc. Circulatory levels
                      of the three cognate ligands for CCR5 (CCL3, CCL4, CCL5)
                      were analysed in sera of breast cancer patients using
                      ELISA.We found that blockade of CCR5 attenuated the
                      proliferation, colony formation and migration of metastatic
                      breast cancer cells, and induced apoptosis and arrest in the
                      G1 phase of the cell cycle. Expression profiling highlighted
                      the involvement of cell cycle related signalling cascades.
                      We also found that treatment with maraviroc significantly
                      inhibited bone metastasis in nude rats implanted with
                      MDA-MB-231 breast cancer cells. Finally, we found that the
                      circulatory levels of three cognate ligands for the CCR5
                      receptor varied between breast cancer patients and healthy
                      controls.Our findings indicate that targeting CCR5 may be an
                      effective strategy to combat breast cancer bone metastasis.},
      cin          = {G401},
      ddc          = {610},
      cid          = {I:(DE-He78)G401-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30456574},
      doi          = {10.1007/s13402-018-0415-3},
      url          = {https://inrepo02.dkfz.de/record/142993},
}