{"entity": "researcher", "timestamp": "2026-04-12T03:36:07.254Z", "family": "Malanchi", "given": "Ilaria", "initials": "I", "orcid": "0000-0003-4867-3311", "affiliations": ["The Francis Crick Institute, London, UK."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/7b2a177fdd084ba88486b18ca508d231.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/7b2a177fdd084ba88486b18ca508d231"}}, "publications": [{"entity": "publication", "iuid": "b286c12a79af41768be6da62ae5271c8", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/b286c12a79af41768be6da62ae5271c8.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/b286c12a79af41768be6da62ae5271c8"}}, "title": "A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation resulting in pro-metastatic NF-\u03baB signaling.", "authors": [{"family": "Altea-Manzano", "given": "Patricia", 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"initials": "V", "orcid": "0000-0002-4090-718X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8b7ec92cacb442749cee18c474e4573d.json"}}, {"family": "Gr\u00fcnewald", "given": "Thomas G P", "initials": "TGP", "orcid": "0000-0003-0920-7377", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f7d1c5a1b0c94ede884388c2e86503f1.json"}}, {"family": "Ben-David", "given": "Uri", "initials": "U", "orcid": "0000-0001-7098-2378", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b88b311ac57b45afb37e8ba5e253191a.json"}}, {"family": "Desmedt", "given": "Christine", "initials": "C", "orcid": "0000-0002-5223-5579", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b7a7cb14a2ab4c55a3a23ed8e4323395.json"}}, {"family": "Malanchi", "given": "Ilaria", "initials": "I", "orcid": "0000-0003-4867-3311", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/7b2a177fdd084ba88486b18ca508d231.json"}}, {"family": "Fendt", "given": "Sarah-Maria", "initials": "SM", "orcid": "0000-0001-6018-9296", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5269066243ec45129407a6340bb437cc.json"}}], "type": "journal article", "published": "2023-03-00", "journal": {"title": "Nat Cancer", "issn": "2662-1347", "volume": "4", "issue": "3", "pages": "344-364", "issn-l": null}, "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.", "doi": "10.1038/s43018-023-00513-2", "pmid": "36732635", "labels": {"SciLifeLab Fellow": null, "Vicent Pelechano": null}, "xrefs": [{"db": "pii", "key": "10.1038/s43018-023-00513-2"}], "notes": [], "created": "2023-05-29T07:36:16.305Z", "modified": "2023-05-29T07:36:17.332Z"}]}