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@ARTICLE{RiosGarcia:131606,
      author       = {M. Rios Garcia and B. Steinbauer$^*$ and K. Srivastava$^*$
                      and M. Singhal$^*$ and F. Mattijssen and A. Maida and S.
                      Christian and H. Hess-Stumpp and H. Augustin$^*$ and K.
                      Müller-Decker$^*$ and P. P. Nawroth and S. Herzig and M.
                      Berriel Diaz},
      title        = {{A}cetyl-{C}o{A} {C}arboxylase 1-{D}ependent {P}rotein
                      {A}cetylation {C}ontrols {B}reast {C}ancer {M}etastasis and
                      {R}ecurrence.},
      journal      = {Cell metabolism},
      volume       = {26},
      number       = {6},
      issn         = {1550-4131},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2017-06238},
      pages        = {842 - 855.e5},
      year         = {2017},
      abstract     = {Breast tumor recurrence and metastasis represent the main
                      causes of cancer-related death in women, and treatments are
                      still lacking. Here, we define the lipogenic enzyme
                      acetyl-CoA carboxylase (ACC) 1 as a key player in breast
                      cancer metastasis. ACC1 phosphorylation was increased in
                      invading cells both in murine and human breast cancer,
                      serving as a point of convergence for leptin and
                      transforming growth factor (TGF) β signaling. ACC1
                      phosphorylation was mediated by TGFβ-activated kinase
                      (TAK) 1, and ACC1 inhibition was indispensable for the
                      elevation of cellular acetyl-CoA, the subsequent increase in
                      Smad2 transcription factor acetylation and activation, and
                      ultimately epithelial-mesenchymal transition and metastasis
                      induction. ACC1 deficiency worsened tumor recurrence upon
                      primary tumor resection in mice, and ACC1 phosphorylation
                      levels correlated with metastatic potential in breast and
                      lung cancer patients. Given the demonstrated effectiveness
                      of anti-leptin receptor antibody treatment in halting
                      ACC1-dependent tumor invasiveness, our work defines a
                      'metabolocentric' approach in metastatic breast cancer
                      therapy.},
      cin          = {A190 / W420},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331 / I:(DE-He78)W420-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29056512},
      doi          = {10.1016/j.cmet.2017.09.018},
      url          = {https://inrepo02.dkfz.de/record/131606},
}