<HashMap><database>biostudies-arrayexpress</database><scores/><additional><submitter>Twan van den Beucken</submitter><organism>Homo sapiens</organism><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16713</full_dataset_link><description>RNA sequencing was performed to characterize transcriptomic changes in the human hepatocellular carcinoma cell line HepG2 following treatment with doxorubicin (DOX), either alone or in combination with the histone deacetylase inhibitors valproic acid (VPA) or suberoylanilide hydroxamic acid (SAHA), relative to untreated controls.  HepG2 cells were exposed to the indicated treatments for 48 hours. Total RNA was extracted, and poly(A)-enriched stranded libraries were prepared. Paired-end sequencing was conducted on an Illumina platform. Reads were aligned to the human reference genome (GRCh38), followed by gene-level quantification and differential gene expression analysis.  This dataset enables analysis of transcriptional programs associated with HDAC inhibition and modulation of DOX response, including pathways related to DNA repair, stress response, and p53 signaling.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Library Construction - Poly(A) libraries were generated using the Zephyr G3® NGS automated system with the NEXTFLEX® Rapid Directional RNA-Seq Kit 2.0 (NOVA-5198–02, PerkinElmer). Library preparation included NEXTFLEX® Poly(A) Beads 2.0 (NOVA-512992, PerkinElmer) for mRNA enrichment and NEXTFLEX® Unique Dual Index Barcodes (NOVA-512923, PerkinElmer) for sample multiplexing. Each library was prepared using 100 ng of total RNA as input, with RNA integrity numbers (RIN ≥ 8). A total of 13 PCR cycles were performed during library amplification.</sample_protocol><sample_protocol>Sample Collection - After the exposure, cells were washed once with PBS and subsequently lysed in 0.5 mL QIAzol Lysis Reagent (79306, Qiagen).</sample_protocol><sample_protocol>Sequencing - Sequencing was carried out on the Illumina NovaSeq 6000 using an S1 flow cell, generating paired-end reads with 100 cycles per read.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Total RNA was extracted using chloroform and isopropanol precipitation.</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>Processed Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><data_protocol>Data Transformation - Raw sequencing reads were quality-checked and aligned to the reference genome using STAR. Gene-level count matrices were generated and imported into DESeq2 for normalization. Size-factor normalization was performed using the median-of-ratios method to correct for library size and compositional differences.</data_protocol><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><instrument_platform>Illumina NovaSeq 6000</instrument_platform><study_type>RNA-seq of coding RNA</study_type><species>Homo sapiens</species><pubmed_authors>Twan van den Beucken</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNA-seq of human liver cancer cell line HepG2 treated with doxorubicin alone or in combination with valproic acid or suberoylanilide hydroxamic acid against untreated controls</name><description>RNA sequencing was performed to characterize transcriptomic changes in the human hepatocellular carcinoma cell line HepG2 following treatment with doxorubicin (DOX), either alone or in combination with the histone deacetylase inhibitors valproic acid (VPA) or suberoylanilide hydroxamic acid (SAHA), relative to untreated controls.  HepG2 cells were exposed to the indicated treatments for 48 hours. Total RNA was extracted, and poly(A)-enriched stranded libraries were prepared. Paired-end sequencing was conducted on an Illumina platform. Reads were aligned to the human reference genome (GRCh38), followed by gene-level quantification and differential gene expression analysis.  This dataset enables analysis of transcriptional programs associated with HDAC inhibition and modulation of DOX response, including pathways related to DNA repair, stress response, and p53 signaling.</description><dates><release>2026-03-24T00:00:00Z</release><modification>2026-03-24T09:34:01.599Z</modification><creation>2026-03-03T12:04:47.71Z</creation></dates><accession>E-MTAB-16713</accession><cross_references><ENA>ERP189827</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003816</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>