Differential transcriptomic modulation by histone deacetylase inhibitor SAHA in LUAD and LUSC.

ABSTRACT:

Background

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.

Methods

LUAD-like NCI-H1299 (TP53^del, NRAS^Q61K) and LUSC-like NCI-H1703 (TP53^WT, PDGFRA^amp, PIK3CA^E542K) cells were treated with SAHA (10 µM, 24 h) or DMSO. Bulk RNA-seq data were analysed with edgeR (FDR < 0.05, |log

SUBMITTER: Wang F 

PROVIDER: S-EPMC12918457 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature