biostudies-arrayexpressReo MaruyamaHomo sapienshttps://www.ebi.ac.uk/biostudies/studies/E-MTAB-16777Biological relevance: This study aims to evaluate how G9a inhibition via BIX01294 affects the chromatin landscape in the context of ARID1A deficiency. We investigated whether the loss of the SWI/SNF subunit ARID1A alters the cellular response to G9a pharmacological targeting in ovarian cancer. Experimental workflow: Human ovarian cancer cell line TOV112D was transduced with shRNA against ARID1A or a non-targeting control. These cells were subsequently treated with the G9a inhibitor BIX01294 or DMSO. Chromatin accessibility was profiled using ATAC-seq to compare the epigenetic changes across these conditions.biostudies-arrayexpressLibrary Construction - Libraries were assembled using the Omni-ATAC protocol26. Briefly, 50,000 cells were lysed in ice-cold ATAC-Resuspension Buffer for 3 minutes to isolate nuclei, which were then subjected to a transposition reaction with Tn5 transposase (Illumina, San Diego, CA, USA) at 37 ℃ for 30 minutes. After purification using the Zymo DNA Clean and Concentrator-5 Kit, the transposed DNA fragments underwent an initial amplification of five cycles, were quantified via real-time polymerase chain reaction, and were subsequently amplified using the NEBNext High-Fidelity 2X PCR Master Mix (New England Biolabs).Sample Collection - TOV112D cells transduced with either shScramble or shARID1A were used to construct the ATAC-seq library.Sequencing - Libraries were sequenced on an Illumina NextSeq 550 platform (Illumina) with paired-end reads (read 1, 75 bp; index 1, 8 bp; index 2, 8 bp, read 2, 75 bp).Nucleic Acid Extraction - Libraries were assembled using the Omni-ATAC protocol26. Briefly, 50,000 cells were lysed in ice-cold ATAC-Resuspension Buffer for 3 minutes to isolate nucleiOrganizationMINSEQE ScoreAssays and DataProcessed DataMAGE-TAB FilesSequence Alignment - For data processing, alignment, and peak calling of ATAC-seq data, the PEPATAC pipeline (http://pepatac.databio.org/en/latest/) was employed. Fastq files were processed to remove Illumina Nextera adapter sequence using Skewer29, with the parameters “-f sanger -t 20 -m pe -x.” Following trimming, the sequencing quality was verified using FastQC. Reads mapping to mitochondrial DNA or repetitive elements were excluded by pre-alignment filtering using Bowtie2 with the parameters “-k 1 -D 20 -R 3 -N 1 -L 20 -I S,1,0.50 -X 2000 --no-mixed --no-discordant”. The remaining reads were aligned to the hg38 human reference genome using Bowtie2 with the options “--very-sensitive -X 2000 --no-mixed --no-discordant.”Data Transformation - Duplicate reads were excluded using Picard’s MarkDuplicates tool (http://broadinstitute.github.io/picard/) with the options “VALIDATION_STRINGENCY=LENIENT REMOVE_DUPLICATES=true”. The final aligned and de-duplicated bam files were utilized for peak calling using MACS2 with “--shift -75 --extsize 150 --nomodel --call-summits --nolambda --keep-dup all.”UnknownTranscriptomicsGenomicsProteomicsNextSeq 550ATAC-seqHomo sapiensReo MaruyamafalseATAC-seq analysis of ARID1A-deficient TOV112D human ovarian cancer cells treated with the G9a inhibitor BIX01294Biological relevance: This study aims to evaluate how G9a inhibition via BIX01294 affects the chromatin landscape in the context of ARID1A deficiency. We investigated whether the loss of the SWI/SNF subunit ARID1A alters the cellular response to G9a pharmacological targeting in ovarian cancer. Experimental workflow: Human ovarian cancer cell line TOV112D was transduced with shRNA against ARID1A or a non-targeting control. These cells were subsequently treated with the G9a inhibitor BIX01294 or DMSO. Chromatin accessibility was profiled using ATAC-seq to compare the epigenetic changes across these conditions.2026-03-20T00:00:00Z2026-03-20T06:41:39.551Z2026-03-19T10:11:51.389ZE-MTAB-16777ERP191005EFO_0002944EFO_0007045EFO_0004170EFO_0004917EFO_0005518EFO_0003816EFO_0004184