High-fat diet and the secretome of breast tumors prime distant organs for metastasis formation. During lung priming, alveolar type II cells increase the release of palmitate, which is oxidized to acetyl-CoA by metastasizing breast cancer cells, where the increased acetylation of the NF-κB subunit p65 activates a pro-metastatic transcriptional program.
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This is a summary of: Altea-Manzano, P. et al. A palmitate-rich metastatic niche enables metastasis growth via p65 acetylation resulting in pro-metastatic NF-κB signaling. Nat. Cancer https://doi.org/10.1038/s43018-023-00513-2 (2023).
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Palmitate oxidation drives a pro-metastatic post-translational modification. Nat Cancer 4, 315–316 (2023). https://doi.org/10.1038/s43018-023-00514-1
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DOI: https://doi.org/10.1038/s43018-023-00514-1