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@ARTICLE{Sjberg:144169,
      author       = {E. Sjöberg and M. Meyrath and L. Milde$^*$ and M. Herrera
                      and J. Lövrot and D. Hägerstrand and O. Frings and M.
                      Bartish and C. Rolny and E. Sonnhammer and A. Chevigné and
                      M. Augsten and A. Östman},
      title        = {{A} {N}ovel {ACKR}2-{D}ependent {R}ole of
                      {F}ibroblast-{D}erived {CXCL}14 in
                      {E}pithelial-to-{M}esenchymal {T}ransition and {M}etastasis
                      of {B}reast {C}ancer.},
      journal      = {Clinical cancer research},
      volume       = {25},
      number       = {12},
      issn         = {1557-3265},
      address      = {Philadelphia, Pa. [u.a.]},
      publisher    = {AACR},
      reportid     = {DKFZ-2019-01718},
      pages        = {3702 - 3717},
      year         = {2019},
      abstract     = {Fibroblasts expressing the orphan chemokine CXCL14 have
                      been previously shown to associate with poor breast cancer
                      prognosis and promote cancer growth. This study explores the
                      mechanism underlying the poor survival associations of
                      stromal CXCL14.Tumor cell epithelial-to-mesenchymal
                      transition (EMT), invasion, and metastasis were studied in
                      in vitro and in vivo models together with fibroblasts
                      overexpressing CXCL14. An approach for CXCL14 receptor
                      identification included loss-of-function studies followed by
                      molecular and functional endpoints. The clinical relevance
                      was further explored in publicly available gene expression
                      datasets.CXCL14 fibroblasts stimulated breast cancer EMT,
                      migration, and invasion in breast cancer cells and in a
                      xenograft model. Furthermore, tumor cells primed by CXCL14
                      fibroblasts displayed enhanced lung colonization after
                      tail-vein injection. By loss-of function experiments, the
                      atypical G-protein-coupled receptor ACKR2 was identified to
                      mediate CXCL14-stimulated responses. Downregulation of
                      ACKR2, or CXCL14-induced NOS1, attenuated the pro-EMT and
                      migratory capacity. CXCL14/ACKR2 expression correlated with
                      EMT and survival in gene expression datasets.Collectively,
                      the findings imply an autocrine fibroblast CXCL14/ACKR2
                      pathway as a clinically relevant stimulator of EMT, tumor
                      cell invasion, and metastasis. The study also identifies
                      ACKR2 as a novel mediator for CXCL14 function and thereby
                      defines a pathway with drug target potential.See related
                      commentary by Zhang et al., p. 3476.},
      keywords     = {CXCL14 protein, human (NLM Chemicals) / Chemokines, CXC
                      (NLM Chemicals)},
      cin          = {A190},
      ddc          = {610},
      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:30850359},
      doi          = {10.1158/1078-0432.CCR-18-1294},
      url          = {https://inrepo02.dkfz.de/record/144169},
}