{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang F"],"funding":["The National Natural Science Foundation of China"],"pagination":["35"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12918457"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["18(1)"],"pubmed_abstract":["<h4>Background</h4>Histone deacetylases (HDACs) are central epigenetic regulators in non-small cell lung cancer (NSCLC), yet responses to HDAC inhibitors (HDACi) vary markedly between lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC). We asked how the pan-HDAC inhibitor suberoylanilide hydroxamic acid (SAHA, vorinostat) rewires lineage-specific transcriptional programs and whether SAHA-aligned modules of genes, rather than individual loci, capture clinically relevant vulnerabilities in each subtype.<h4>Methods</h4>LUAD-like NCI-H1299 (TP53<sup>del</sup>, NRAS<sup>Q61K</sup>) and LUSC-like NCI-H1703 (TP53<sup>WT</sup>, PDGFRA<sup>amp</sup>, PIK3CA<sup>E542K</sup>) cells were treated with SAHA (10 µM, 24 h) or DMSO. Bulk RNA-seq data were analysed with edgeR (FDR < 0.05, |log<sub"],"journal":["Clinical epigenetics"],"pubmed_title":["Differential transcriptomic modulation by histone deacetylase inhibitor SAHA in LUAD and LUSC."],"pmcid":["PMC12918457"],"funding_grant_id":["82070406, 82072047, and 82170008"],"pubmed_authors":["Wang C","Fu X","Ma X","Wang F","Lin Y","Cen H","Zhang L","Su J","Shu L","Huang Y","Guan X","Yang Q","You G","Yu XY"],"additional_accession":[]},"is_claimable":false,"name":"Differential transcriptomic modulation by histone deacetylase inhibitor SAHA in LUAD and LUSC.","description":"<h4>Background</h4>Histone deacetylases (HDACs) are central epigenetic regulators in non-small cell lung cancer (NSCLC), yet responses to HDAC inhibitors (HDACi) vary markedly between lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC). We asked how the pan-HDAC inhibitor suberoylanilide hydroxamic acid (SAHA, vorinostat) rewires lineage-specific transcriptional programs and whether SAHA-aligned modules of genes, rather than individual loci, capture clinically relevant vulnerabilities in each subtype.<h4>Methods</h4>LUAD-like NCI-H1299 (TP53<sup>del</sup>, NRAS<sup>Q61K</sup>) and LUSC-like NCI-H1703 (TP53<sup>WT</sup>, PDGFRA<sup>amp</sup>, PIK3CA<sup>E542K</sup>) cells were treated with SAHA (10 µM, 24 h) or DMSO. Bulk RNA-seq data were analysed with edgeR (FDR < 0.05, |log<sub","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-07-09T11:32:07.297Z","creation":"2026-07-09T10:49:42.942Z"},"accession":"S-EPMC12918457","cross_references":{"pubmed":["41593801"],"doi":["10.1186/s13148-026-02051-x"]}}