ArticleNature communications2026
BCAT1 inhibits crotonate-related epigenetic modulation of metabolic genes in tumor-associated macrophages to counter immunosuppression.
Article in Nature communications, 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
The heterogeneous and immunosuppressive tumor microenvironment (TME) in hepatocellular carcinoma (HCC) contributes to poor immunotherapy responses. Tumor-associated macrophages (TAM) are central to the immunosuppressive TME, but how metabolic programs regulate TAM pro-tumorigenic functions remain incompletely understood. Here, we identify branched-chain amino acid transaminase 1 (BCAT1) as a metabolic checkpoint in TAMs constraining tumor progression. Compared with wild-type TAMs, BCAT1-deficient TAMs have increased intracellular crotonate, as well as enhanced histone H3 lysine 14 crotonylation, upregulated lipid metabolism genes and an immunosuppressive phenotype. In HCC mouse models, BCAT1-deficient TAMs aggravate tumor burden and suppress CD8
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