{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE322nnn/GSE322742/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE322742"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptional profiling of sorafenib-resistant and parental sensitive HepG2 and Huh7 hepatocellular carcinoma cells","description":"Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide, and acquired resistance to sorafenib—the first-line targeted therapy for advanced HCC—remains a major clinical challenge. To investigate the molecular mechanisms underlying sorafenib resistance in HCC, we established sorafenib-resistant sublines of HepG2 and Huh7 cells through continuous exposure to increasing concentrations of sorafenib. We then performed RNA-seq analysis comparing these resistant sublines with their parental sensitive counterparts. Differential gene expression analysis revealed distinct transcriptional signatures associated with sorafenib resistance. Our findings provide a comprehensive transcriptomic resource for understanding sorafenib resistance mechanisms and identify potential candidate genes that may serve as biomarkers or therapeutic targets for overcoming drug resistance in HCC.","dates":{"publication":"2026/06/10"},"accession":"GSE322742","cross_references":{"GSM":["GSM9557560","GSM9557554","GSM9557553","GSM9557556","GSM9557555","GSM9557558","GSM9557557","GSM9557559"],"GPL":["24676"],"GSE":["322742"],"taxon":["Homo sapiens"],"PMID":["[42026022]"]}}