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@ARTICLE{AlteaManzano:241155,
      author       = {P. Altea-Manzano and G. Doglioni and Y. Liu and A. M.
                      Cuadros and E. Nolan and J. Fernández-García and Q. Wu and
                      M. Planque and K. J. Laue and F. Cidre-Aranaz$^*$ and X.-Z.
                      Liu and O. Marin-Bejar and J. Van Elsen and I. Vermeire and
                      D. Broekaert and S. Demeyer and X. Spotbeen and J. Idkowiak
                      and A. Montagne and M. Demicco and H. F. Alkan and N. Rabas
                      and C. Riera-Domingo and F. Richard and T. Geukens and M. De
                      Schepper and S. Leduc and S. Hatse and Y. Lambrechts and E.
                      J. Kay and S. Lilla and A. Alekseenko and V. Geldhof and B.
                      Boeckx and C. de la Calle Arregui and G. Floris and J. V.
                      Swinnen and J.-C. Marine and D. Lambrechts and V. Pelechano
                      and M. Mazzone and S. Zanivan and J. Cools and H. Wildiers
                      and V. Baud and T. Grünewald$^*$ and U. Ben-David and C.
                      Desmedt and I. Malanchi and S.-M. Fendt},
      title        = {{A} palmitate-rich metastatic niche enables metastasis
                      growth via p65 acetylation resulting in pro-metastatic
                      {NF}-κ{B} signaling.},
      journal      = {Nature cancer},
      volume       = {4},
      number       = {3},
      issn         = {2662-1347},
      address      = {London},
      publisher    = {Nature Research},
      reportid     = {DKFZ-2023-00263},
      pages        = {344-364},
      year         = {2023},
      note         = {2023 Mar;4(3):344-364},
      abstract     = {Metabolic rewiring is often considered an adaptive pressure
                      limiting metastasis formation; however, some nutrients
                      available at distant organs may inherently promote
                      metastatic growth. We find that the lung and liver are
                      lipid-rich environments. Moreover, we observe that
                      pre-metastatic niche formation increases palmitate
                      availability only in the lung, whereas a high-fat diet
                      increases it in both organs. In line with this, targeting
                      palmitate processing inhibits breast cancer-derived lung
                      metastasis formation. Mechanistically, breast cancer cells
                      use palmitate to synthesize acetyl-CoA in a carnitine
                      palmitoyltransferase 1a-dependent manner. Concomitantly,
                      lysine acetyltransferase 2a expression is promoted by
                      palmitate, linking the available acetyl-CoA to the
                      acetylation of the nuclear factor-kappaB subunit p65.
                      Deletion of lysine acetyltransferase 2a or carnitine
                      palmitoyltransferase 1a reduces metastasis formation in lean
                      and high-fat diet mice, and lung and liver metastases from
                      patients with breast cancer show coexpression of both
                      proteins. In conclusion, palmitate-rich environments foster
                      metastases growth by increasing p65 acetylation, resulting
                      in a pro-metastatic nuclear factor-kappaB signaling.},
      cin          = {B410 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)B410-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36732635},
      doi          = {10.1038/s43018-023-00513-2},
      url          = {https://inrepo02.dkfz.de/record/241155},
}