{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE336nnn/GSE336084/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336084"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"TIMELESS promotes glioma stemness and malignancy through JAK-STAT3 pathway","description":"RNA-sequencing (RNA-seq) analysis was performed to identify TIMELESS-regulated gene signatures in mouse glioblastoma (GBM) CT2A cells. Timeless was originally identified as a core component of the circadian clock machinery, but its role in GBM stemness and malignancy has not been defined. To investigate the mechanisms underlying Timeless-driven GBM malignancy, we generated CT2A cells with stable Timeless knockdown (KD) using a lentivirus expressing Timeless- specific shRNA, alongside CT2A cells transduced with a non-targeting scramble shRNA (shScramble) as a control. Total RNA was extracted from three independent biological replicates of shScramble and Timeless-KD CT2A cells, and bulk RNA barcoding and sequencing (BRB-seq) libraries were prepared and sequenced on the Illumina NextSeq2000 platform. Among the genes detected, genes whose mean expression levels in Timeless-KD cells were reduced to half or less of those in shScramble cells were selected and subjected to enrichment analysis using ShinyGO, which revealed significant enrichment of stem cell- related gene signatures. These findings suggest that TIMELESS regulates cancer stem-like properties of GBM cells.","dates":{"publication":"2026/09/01"},"accession":"GSE336084","cross_references":{"GSM":["GSM9826867","GSM9826866"],"GPL":["30172"],"GSE":["336084"],"taxon":["Mus musculus"]}}