ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University
[Hepatocellular carcinoma-derived lactate-mediated histone H3K18 lactylation modifies S100A2 transcription to promote proliferation, migration, invasion and epithelial-mesenchymal transition of hepatocellular carcinoma cells].
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University. 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
objectivesTo investigate the role of histone H3 lysine 18 lactylation (H3K18la) regulating the transcription of S100 calcium-binding protein A2 (S100A2) in the development of hepatocellular carcinoma (HCC) and its molecular mechanism.
methodsHCC single-cell transcriptome sequencing data were used to screen the differentially expressed genes and pathways. Intracellular lactate and histone lactylation were measured in HCC and normal hepatocyte cell lines. The effects of glycolysis inhibitors (2-DG/Oxamate) on proliferation, migration, and invasion of the cells were evaluated, and ChIP-qPCR was used to detect the enrichment of H3K18la at the
resultsGlycolysis and pyruvate metabolism pathways were upregulated in HCC, and lactate levels was elevated in HCC cells. Pan-Kla and H3K18la were significantly overexpressed in HCC cell lines, especially under hypoxia. Glycolysis inhibitors dose-dependently reduced H3K18la and suppressed malignant phenotypes of HCC cells. S100A2 mRNA and protein levels were upregulated in HCC, and its high expression was correlated with poor prognosis. S100A2 promoted HCC cell proliferation, migration, and invasion, which were reversed by 2‑DG. S100A2 directly interacted with KRT6A, the expression of nuclear β‑catenin was reduced after
conclusionsHCC-derived lactate enhances H3K18la modification, which activates
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