{"database":"GEO","file_versions":[],"scores":null,"additional":{"omics_type":["Other"],"species":["Homo sapiens"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE304150"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Activation of the aryl hydrocarbon receptor in human melanoma cells enhances cancer cell-intrinsic MHC-II expression [Genome-wide CRISPR screen]","description":"Cancer immunotherapy has revolutionized patient outcomes by enhancing immune responses, with major histocompatibility complex class II (MHC-II) playing a pivotal role. While MHC-II is classically expressed by professional antigen-presenting cells (pAPCs), emerging evidence highlights its expression by cancer cells, where it correlates with enhanced immune infiltration and favorable clinical outcomes. However, the regulatory mechanisms of cancer cell-intrinsic MHC-II remain unclear. Here, using genome-wide CRISPR-Cas9 screens, we identify the aryl hydrocarbon receptor (AhR) and its nuclear translocator (ARNT) as key regulators of MHC-II expression in human melanoma cells. The expression level and ligand-dependent activity of AhR and ARNT significantly correlate with cancer cell-intrinsic MHC-II expression. Multi-omics analyses reveal that this regulation is mediated through transcriptional activation of the MHC-II transactivator, CIITA, via binding of AhR-ARNT to its second promoter, pII. Our findings uncover a previously unrecognized regulatory axis for MHC-II expression in tumors, presenting new targets for enhancing immunotherapy.","dates":{"publication":"2026/04/01"},"accession":"GSE304150","cross_references":{"GSM":["GSM9144388","GSM9144389","GSM9144386","GSM9144387","GSM9144384","GSM9144385","GSM9144383","GSM9144391","GSM9144392","GSM9144390"],"GPL":["20795"],"GSE":["304150"],"taxon":["Homo sapiens"],"PMID":["[41721339]"]}}