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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},
}