ArticleScientific reports2026
LDHA-driven ACAA2 lactylation at K270 reprograms fatty acid metabolism to promote clear cell renal cell carcinoma progression.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study elucidates a novel lactate dehydrogenase A (LDHA)-acetyl CoA acyltransferase 2 (ACAA2)-lactylation axis driving clear cell renal cell carcinoma (ccRCC) progression through metabolic reprogramming. LDHA upregulation in ccRCC tissues is clinically linked to shorter overall patient survival. Functional assays demonstrated that LDHA overexpression enhances ccRCC proliferation, migration, and invasion, while knockdown attenuated these effects. Lactylome profiling identified 59 modified sites and revealed ACAA2 K270 lactylation (ACAA2-K270la) as a key regulator. Structural and biochemical analyses revealed K270 lactylation increases ACAA2 activity, promoting free fatty acids (FFAs) elevation. Exogenous FFAs recapitulated pro-tumorigenic effects in a dose-dependent manner. Mechanistically, LDHA-mediated ACAA2-K270la upregulated cyclins and cyclin-dependent kinases (CDKs), linking metabolic rewiring to cell cycle progression. These findings establish lactylation as a critical metabolic checkpoint in ccRCC, and reveal new therapeutic targets for metabolic intervention.
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