{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["SOURA CHAKRABORTY"],"instrument_platform":["Qiagen RNA extraction kit","Illumina NovaSeq 6000","Novogene automated library prep system"],"study_type":["RNA-seq of coding RNA"],"organism":["Homo sapiens"],"species":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16367"],"description":["Steroids enriched within the lung tumor microenvironment suppress the cytotoxic activity of tumor-infiltrating NK cells and intensify hypoxic stress. To model these conditions in vitro, CEACAM5-specific CAR-NK cells and NR3C1-knockout CAR-NK cells were exposed to hydrocortisone (1 µM), hypoxia-mimicking CoCl₂ (100 µM), or their combination. NK cells were treated for 24 hours, followed by a 6-hour co-culture with A549 lung cancer cells to activate NK-cell effector programs. After co-culture, NK cells were isolated to high purity and subjected to bulk RNA sequencing to characterize transcriptional changes driven by steroid signalling, hypoxia, and glucocorticoid receptor deficiency. This dataset includes multiple treatment groups: untreated CAR-NK cells, hypoxia-treated CAR-NK cells, combined hypoxia + hydrocortisone–treated CAR-NK cells, and corresponding NR3C1-knockout CAR-NK cell groups under identical conditions."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Library Construction - RNA-seq libraries were sequenced by Novogene using an Illumina platform, generating paired-end reads. Standard Illumina sequencing chemistry and quality control procedures were applied. Raw FASTQ files were delivered after base calling, filtering, and adapter trimming performed by Novogene.","Sample Collection - CAR-NK-92, and NR3C1-knockout CAR-NK-92 cells were cultured under defined experimental conditions. Cells were treated with hydrocortisone and/or CoCl₂ and subsequently co-cultured with A549 target cells for 6 hours. Following co-culture, NK-92 cells were collected, washed in cold PBS, and pelleted in RNase-free tubes. Cell pellets were processed immediately for RNA extraction.","Sequencing - Libraries were sequenced by Novogene on an Illumina NovaSeq platform using paired-end (typically 150 bp) chemistry. Standard Illumina base-calling and quality filtering workflows were applied. Clean FASTQ files were delivered after adapter removal and low-quality read filtering.","Nucleic Acid Extraction - Total RNA was extracted from sorted NK cells using the Qiagen RNA extraction kit following the manufacturer’s instructions (including on-column DNase digestion when applicable). RNA quantity and purity were assessed using NanoDrop spectrophotometry. High-quality RNA (RIN ≥ 7) was used for downstream library preparation."],"figure_sub":["Organization","MINSEQE Score","Assays and Data","MAGE-TAB Files"],"pubmed_authors":["SOURA CHAKRABORTY"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptomic profiling of CAR-NK and NR3C1-knockout CAR-NK cells exposed to hydrocortisone and hypoxia-mimicking conditions","description":"Steroids enriched within the lung tumor microenvironment suppress the cytotoxic activity of tumor-infiltrating NK cells and intensify hypoxic stress. To model these conditions in vitro, CEACAM5-specific CAR-NK cells and NR3C1-knockout CAR-NK cells were exposed to hydrocortisone (1 µM), hypoxia-mimicking CoCl₂ (100 µM), or their combination. NK cells were treated for 24 hours, followed by a 6-hour co-culture with A549 lung cancer cells to activate NK-cell effector programs. After co-culture, NK cells were isolated to high purity and subjected to bulk RNA sequencing to characterize transcriptional changes driven by steroid signalling, hypoxia, and glucocorticoid receptor deficiency. This dataset includes multiple treatment groups: untreated CAR-NK cells, hypoxia-treated CAR-NK cells, combined hypoxia + hydrocortisone–treated CAR-NK cells, and corresponding NR3C1-knockout CAR-NK cell groups under identical conditions.","dates":{"release":"2025-12-18T00:00:00Z","modification":"2025-12-18T16:39:36.524Z","creation":"2025-12-10T09:41:43.016Z"},"accession":"E-MTAB-16367","cross_references":{"ENA":["ERP186341"],"EFO":["EFO_0002944","EFO_0004170","EFO_0005518","EFO_0003738","EFO_0004184"]}}