{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE309nnn/GSE309650/"]},"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=GSE309650"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Context-dependent effect of glucocorticoid receptor activity shapes ovarian cancer cell plasticity and therapy response","description":"The phenotypic plasticity of cancer cells, i.e. their adaptability to a variable/ stressful environment, is fundamental for disease progression/aggressiveness. Here we revealed that the glucocorticoid receptor (GR, NR3C1), a key player in the human response to stress, controls proliferation, morphology, motility/invasion, and the gene expression profile of high-grade serous ovarian carcinoma (hereafter OC) cells. By modulating glucose metabolism, GR acts as a tumor suppressor delaying ovarian cancer growth under 3D-settings. Conversely, under 2D conditions GR acts as a tumor promoter, driving cell mesenchymalization, increasing cell motility and chemoresistance. Strikingly, modulators of glucose metabolism as metformin and 2-deoxyglucose, are alone sufficient to induce similar cell behavioural changes. So, in ovarian cancer a GR-glucose metabolism axis modulates a escaping signalling response triggered by stressful (3D overgrowth, starvation) condition.","dates":{"publication":"2026/03/04"},"accession":"GSE309650","cross_references":{"GSM":["GSM9271165","GSM9271166","GSM9271167","GSM9271168","GSM9271172","GSM9271173","GSM9271174","GSM9271163","GSM9271164","GSM9271170","GSM9271171","GSM9271169"],"GPL":["24676"],"GSE":["309650"],"taxon":["Homo sapiens"]}}