GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE305nnn/GSE305239/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE305239GEOGSEfalseTranscriptomic profiling of STING-agonist-sensitive and resistant glioblastoma cells under acute diABZI stimulation and chronic selectionGlioblastoma (GBM) exhibits profound therapeutic resistance and an immunosuppressive tumor microenvironment. The cGAS–STING pathway is an attractive target, yet sustained pathway activation can trigger adaptive escape. To define tumor-intrinsic adaptations to STING agonists, we generated an isogenic model using H4 GBM cells: (i) parental H4 treated with vehicle (DMSO, 6 h), (ii) parental H4 challenged acutely with diABZI (1 uM, 6 h), and (iii) a resistant subline (H4-R) derived by chronic diABZI dose escalation (up to 20 uM for >2 months) and harvested drug-free. Poly(A) RNA-seq (NovaSeq 6000, paired-end 150 bp) was performed in biological triplicates. Acute STING activation in parental cells induced a stereotypic interferon/chemokine program centered on CXCL10 together with apoptosis-related genes, whereas H4-R showed suppression of DNA-sensing/STING outputs and a shift toward hypoxia/ECM signatures. In functional assays, CXCL10 neutralization reduced STING-agonist efficacy, while recombinant CXCL10 restored responses. Processed results are provided in GEO; raw FASTQ files are in SRA under the linked BioProject. This dataset enables reuse for benchmarking STING biology, chemokine signaling, and resistance mechanisms in GBM.2026/09/01GSE305239GSM9166554GSM9166553GSM9166552GSM9166558GSM9166557GSM9166556GSM9166555GSM9166559GSM916656024676305239Homo sapiens