| Home > Publications database > A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation resulting in pro-metastatic NF-κB signaling. > print |
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| 024 | 7 | _ | |a 10.1038/s43018-023-00513-2 |2 doi |
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| 100 | 1 | _ | |a Altea-Manzano, Patricia |0 0000-0002-7075-2051 |b 0 |
| 245 | _ | _ | |a A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation resulting in pro-metastatic NF-κB signaling. |
| 260 | _ | _ | |a London |c 2023 |b Nature Research |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1680157298_7806 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
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| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 500 | _ | _ | |a 2023 Mar;4(3):344-364 |
| 520 | _ | _ | |a 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. |
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| 700 | 1 | _ | |a Liu, Yawen |b 2 |
| 700 | 1 | _ | |a Cuadros, Alejandro M |0 0000-0002-5900-5143 |b 3 |
| 700 | 1 | _ | |a Nolan, Emma |b 4 |
| 700 | 1 | _ | |a Fernández-García, Juan |0 0000-0003-3422-3627 |b 5 |
| 700 | 1 | _ | |a Wu, Qi |b 6 |
| 700 | 1 | _ | |a Planque, Mélanie |b 7 |
| 700 | 1 | _ | |a Laue, Kathrin Julia |b 8 |
| 700 | 1 | _ | |a Cidre-Aranaz, Florencia |0 P:(DE-HGF)0 |b 9 |
| 700 | 1 | _ | |a Liu, Xiao-Zheng |b 10 |
| 700 | 1 | _ | |a Marin-Bejar, Oskar |0 0000-0002-6889-6566 |b 11 |
| 700 | 1 | _ | |a Van Elsen, Joke |0 0000-0002-7349-043X |b 12 |
| 700 | 1 | _ | |a Vermeire, Ines |0 0000-0003-3366-7410 |b 13 |
| 700 | 1 | _ | |a Broekaert, Dorien |0 0000-0002-9777-1607 |b 14 |
| 700 | 1 | _ | |a Demeyer, Sofie |0 0000-0002-8193-5734 |b 15 |
| 700 | 1 | _ | |a Spotbeen, Xander |b 16 |
| 700 | 1 | _ | |a Idkowiak, Jakub |b 17 |
| 700 | 1 | _ | |a Montagne, Aurélie |b 18 |
| 700 | 1 | _ | |a Demicco, Margherita |0 0000-0002-9396-3281 |b 19 |
| 700 | 1 | _ | |a Alkan, H Furkan |b 20 |
| 700 | 1 | _ | |a Rabas, Nick |b 21 |
| 700 | 1 | _ | |a Riera-Domingo, Carla |0 0000-0001-7277-234X |b 22 |
| 700 | 1 | _ | |a Richard, François |0 0000-0003-4353-3619 |b 23 |
| 700 | 1 | _ | |a Geukens, Tatjana |b 24 |
| 700 | 1 | _ | |a De Schepper, Maxim |b 25 |
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| 700 | 1 | _ | |a Hatse, Sigrid |0 0000-0002-6764-2628 |b 27 |
| 700 | 1 | _ | |a Lambrechts, Yentl |0 0000-0002-9013-8091 |b 28 |
| 700 | 1 | _ | |a Kay, Emily Jane |b 29 |
| 700 | 1 | _ | |a Lilla, Sergio |0 0000-0003-3142-7640 |b 30 |
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| 700 | 1 | _ | |a Geldhof, Vincent |b 32 |
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| 700 | 1 | _ | |a Lambrechts, Diether |0 0000-0002-3429-302X |b 38 |
| 700 | 1 | _ | |a Pelechano, Vicent |0 0000-0002-9415-788X |b 39 |
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| 700 | 1 | _ | |a Cools, Jan |0 0000-0001-6626-5843 |b 42 |
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| 700 | 1 | _ | |a Baud, Véronique |0 0000-0002-4090-718X |b 44 |
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| 700 | 1 | _ | |a Malanchi, Ilaria |0 0000-0003-4867-3311 |b 48 |
| 700 | 1 | _ | |a Fendt, Sarah-Maria |0 0000-0001-6018-9296 |b 49 |
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