ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/007/SRR6705537/SRR6705537_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/001/SRR6705541/SRR6705541_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/000/SRR6705540/SRR6705540_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/008/SRR6705538/SRR6705538_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/009/SRR6705539/SRR6705539_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/000/SRR6705540/SRR6705540_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/007/SRR6705537/SRR6705537_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/001/SRR6705541/SRR6705541_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/009/SRR6705539/SRR6705539_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR670/008/SRR6705538/SRR6705538_2.fastq.gzprimaryOK200GenomicsGenomics, Bioinformatics, The Wistar Institutehttps://www.ebi.ac.uk/ena/browser/view/PRJNA433734Homo sapiensxref:PubMed:30297712The SWI/SNF chromatin remodeling complex is altered in ~20% of human cancers. ARID1A, a component of the SWI/SNF chromatin-remodeling complex, is the most frequently mutated epigenetic regulator in human cancers. Inactivation of the SWI/SNF complex is synthetically lethal with inhibition of EZH2 activity. EZH2 inhibitors are entering clinical trials for specific tumor types with SWI/SNF mutations. However, mechanisms of de novo or acquired resistance to EZH2 inhibitors in cancers with inactivating SWI/SNF mutations are unknown. Here we show that the switch of the SWI/SNF catalytic subunits from SMARCA4 to SMARCA2 drives resistance to EZH2 inhibitors in ARID1A-mutated ovarian cancer cells. Overall design: Parental TOV21G cell line and and resistant to EZH2 inhibitor GSK126 treatment clones were assayed by RNA-seq and BRG1 CHIP-seqENAfalseCatalytic subunits switch drives resistance to EZH2 inhibitors in ARID1A-mutated cells [RNA-seq]Catalytic subunits switch drives resistance to EZH2 inhibitors in ARID1A-mutated cells [RNA-seq]2025-09-242019-02-11PRJNA433734GSE110449960630297712