GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE333nnn/GSE333925/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE333925GEOGSEfalseGene expression profile of 31 RAS/RAF-wild-type colorectal cancer (CRC) stem-cell (SC) spheroids and 7 FGFR-inhibitor resistant CSC-SC spheroidsThis study investigated mechanisms of acquired resistance to FGFR inhibitor therapy in RAS/RAF–wild-type colorectal cancer (CRC). RNA sequencing (RNA-seq) data from 47 RAS/RAF-wild-type colorectal cancer stem-cell (CRC-SC) spheroid lines previously deposited under GSE205787 were integrated with newly generated RNA-seq data from 31 additional RAS/RAF-wild-type CRC-SC spheroid lines and seven FGFR inhibitor-resistant CRC-SC derivatives. The resistant derivatives were established from parental CRC-SC spheroid lines by continuous exposure to erdafitinib or futibatinib. Comparative transcriptomic analysis between matched parental and resistant lines revealed consistent upregulation of EGFR and downregulation of PTPROt, a truncated isoform of PTPRO, in resistant derivatives. Gene set enrichment analysis further indicated activation of EGFR-related signaling pathways in FGFR inhibitor-resistant spheroids. In addition, the integrated RNA-seq dataset comprising 78 RAS/RAF-wild-type CRC-SC lines was used to validate the inverse correlation between EGFR and PTPRO mRNA expression, supporting the involvement of PTPROt downregulation and EGFR pathway activation in acquired resistance to FGFR inhibition.2026/06/09GSE333925GSM9777493GSM9777471GSM9777470GSM9777492GSM9777491GSM9777490GSM9777479GSM9777478GSM9777499GSM9777477GSM9777476GSM9777498GSM9777497GSM9777475GSM9777496GSM9777474GSM9777473GSM9777495GSM9777494GSM9777472GSM9777482GSM9777481GSM9777480GSM9777468GSM9777501GSM9777500GSM9777489GSM9777467GSM9777488GSM9777487GSM9777486GSM9777485GSM9777484GSM9777483GSM9777504GSM9777503GSM9777502GSM977746911154333925Homo sapiens