GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335769/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE335769GEOGSEfalseARID1B loss drives sorafenib resistance through transcriptional reprogramming in hepatocellular carcinomamRNA-seq was performed in HepG2 hepatocellular carcinoma cells to characterize transcriptional changes driven by ARID1B loss under sorafenib treatment. Wild-type (WT) and ARID1B-knockout (ARID1B-KO) HepG2 cells were treated with sorafenib (5 µM, 48 h) or DMSO vehicle, with three biological replicates per condition. DESeq2 interaction model identified ARID1B-dependent transcriptional responses to sorafenib. Preprint: https://doi.org/10.64898/2026.06.11.7317252026/06/19GSE335769GSM9820473GSM9820484GSM9820474GSM9820482GSM9820483GSM9820477GSM9820478GSM9820475GSM9820476GSM9820479GSM9820480GSM982048130882335769Homo sapiens10.64898/2026.06.11.731725