SATB2 Mediates H3K9 Delactylation by Recruiting HDAC3 to Repress LCN2 and Inhibit Lung Tumor Growth and Metastasis - PubMed
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- #LCN2
- #H3K9 delactylation
- #SATB2
- SATB2 acts as a tumor suppressor in NSCLC by inhibiting cell proliferation, migration, invasion, and EMT.
- SATB2 reduces histone H3 lysine 9 lactylation (H3K9la), a novel histone mark in NSCLC, and represses the oncoprotein LCN2.
- SATB2 recruits HDAC3 to the LCN2 promoter, catalyzing H3K9 delactylation to suppress LCN2 transcription.
- Exogenous lactate reverses SATB2-mediated suppression of H3K9la and LCN2, restoring oncogenic phenotypes.
- In vivo, SATB2 overexpression inhibits tumor growth and metastasis, while LCN2 overexpression rescues these effects.
- The study reveals a new epigenetic-metabolic pathway in NSCLC, offering potential therapeutic targets.