{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["SOURA CHAKRABORTY"],"instrument_platform":["BD FACSAria III cell sorter","Illumina NovaSeq 6000","Novogene in-house automated library preparation 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-16373"],"description":["CEACAM5-specific CAR NK-92 cells were engineered to target CEACAM5-expressing lung tumor cells. To study their transcriptional response during tumor engagement, parental NK-92 cells, CEACAM5-CAR NK-92 cells, hydrocortisone-treated CAR NK-92 cells, NR3C1-knockout (cortisol-resistant) CAR NK-92 cells, and hydrocortisone-treated NR3C1-knockout CAR NK-92 cells were co-cultured with CEACAM5⁺ A549 lung cancer cells for 16 hours. Following co-culture, NK-92–derived effector cells were isolated by flow cytometry and processed for bulk RNA sequencing. This dataset captures transcriptional programs associated with CAR activation, hydrocortisone exposure, and glucocorticoid receptor deficiency in NK-92–based effector cells responding to CEACAM5⁺ tumor targets."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Library Construction - RNA-seq libraries were generated by Novogene using their standard mRNA-seq workflow.","Sequencing - Prepared libraries were sequenced by Novogene on an Illumina NovaSeq platform using paired-end sequencing (typically 150 bp). Standard Illumina base-calling, demultiplexing, and quality filtering procedures were applied. Clean FASTQ files were provided after adapter trimming and removal of low-quality reads.","Nucleic Acid Extraction - Total RNA was extracted using the Qiagen RNA extraction kit following the manufacturer’s instructions, including optional on-column DNase digestion. RNA concentration and purity were assessed using NanoDrop. High-quality RNA was used for subsequent library preparation by Novogene.","Sample Collection - NK-92, CAR NK-92, hydrocortisone-treated CAR NK-92, NR3C1-knockout CAR NK-92, and hydrocortisone-treated NR3C1-knockout CAR NK-92 cells were co-cultured with CEACAM5⁺ A549 target cells for 16 hours. After co-culture, NK-92–derived cells were collected by FACS sorting. Sorted cell pellets were immediately processed for RNA extraction."],"figure_sub":["Organization","MINSEQE Score","Assays and Data","MAGE-TAB Files"],"pubmed_authors":["SOURA CHAKRABORTY"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptomic profiling of NK-92, CAR NK-92, and NR3C1-knockout CAR NK-92 cells following co-culture with CEACAM5⁺ A549 lung cancer cells","description":"CEACAM5-specific CAR NK-92 cells were engineered to target CEACAM5-expressing lung tumor cells. To study their transcriptional response during tumor engagement, parental NK-92 cells, CEACAM5-CAR NK-92 cells, hydrocortisone-treated CAR NK-92 cells, NR3C1-knockout (cortisol-resistant) CAR NK-92 cells, and hydrocortisone-treated NR3C1-knockout CAR NK-92 cells were co-cultured with CEACAM5⁺ A549 lung cancer cells for 16 hours. Following co-culture, NK-92–derived effector cells were isolated by flow cytometry and processed for bulk RNA sequencing. This dataset captures transcriptional programs associated with CAR activation, hydrocortisone exposure, and glucocorticoid receptor deficiency in NK-92–based effector cells responding to CEACAM5⁺ tumor targets.","dates":{"release":"2025-12-18T00:00:00Z","modification":"2025-12-18T16:40:44.461Z","creation":"2025-12-09T22:55:59.811Z"},"accession":"E-MTAB-16373","cross_references":{"ENA":["ERP186340"],"EFO":["EFO_0002944","EFO_0004170","EFO_0005518","EFO_0003738","EFO_0004184"]}}