GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE310nnn/GSE310042/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE310042GEOGSEfalseComprehensive transcriptome and epigenome profiling of A2780 models reveals distinct programs of cisplatin, paclitaxel, and dual resistance [RNA-seq]Ovarian cancer is the most lethal gynecologic cancer, largely because most patients eventually relapse after initially responding to platinum- and taxane-based chemotherapy. To understand how cancer cells adapt to these drugs, we generated cisplatin-resistant (CpR), paclitaxel-resistant (TxR), and dual-resistant (TxCpR) derivatives from the parental A2780 cell line and profiled their transcriptomes and chromatin landscapes using RNA-seq and ATAC-seq. The three resistant lines displayed distinct cellular morphologies, gene expression profiles, and chromatin accessibility patterns. Notably, the dual-resistant state was not simply a combination of the cisplatin- and paclitaxel-resistant states but instead represented a unique regulatory configuration. Integrative analysis of RNA-seq and ATAC-seq identified potential regulators associated with specific drug-resistance of A2780. Furthermore, we suggested resistance-specific distal regulatory regions highly related with transcription factors either directly or indirectly involved in cancer progression, cell plasticity and chemotherapy resistance. Our paired RNA-seq and ATAC-seq datasets provide valuable and comprehensive resources for exploring how enhancer–transcription factor interactions drive chemotherapy resistance and for identifying new therapeutic targets in ovarian cancer.2026/08/10GSE310042GSM9287091GSM9287090GSM9287097GSM9287096GSM9287093GSM9287092GSM9287095GSM928709434284310042Homo sapiens