{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335399/"]},"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=GSE335399"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Dimethyl Fumarate Reprograms Liver Cancer Immunity via NF-κB/PD-L1 Suppression and Cuproptosis Induction: A Novel Therapeutic Strategy","description":"Background: Dimethyl fumarate (DMF) possesses immunoregulatory and anti-tumor properties, yet its therapeutic potential in liver cancer remains unexplored. This study aimed to investigate DMF’s role in liver cancer immune regulation and elucidate the underlying molecular mechanisms. Methods: Cell viability, proliferation, and cell cycle were assessed using CCK-8, colony formation, and flow cytometry. NF-κB signaling, cuproptosis-related proteins, and PD-L1 were analyzed by Western blot. Aerobic glycolysis and Oxidative phosphorylation were evaluated via ECAR, OCR, lactate production, glucose consumption, and GAPDH activity. PD-L1, HSP70, and DLAT aggregation were quantified by immunofluorescence. The combined anti-tumor efficacy of DMF and cuproptosis induction was validated in a murine liver cancer model. Results: DMF suppressed liver cancer cell viability, clonogenicity, and cell cycle progression while downregulating PD-L1 expression through NF-κB pathway inhibition. It attenuated aerobic glycolysis and promoted cuproptosis. In tumor-immune cell co-cultures, DMF enhanced dendritic cell and natural killer cell function by dual-targeting NF-κB/PD-L1 and inducing cuproptosis. In vivo, DMF combined with Cu-ES increased immune cell infiltration and significantly inhibited tumor progression. Conclusion: DMF combined with cuproptosis induction remodels the tumor immune microenvironment and represents a novel therapeutic strategy to potentiate immunotherapy efficacy in liver cancer.","dates":{"publication":"2026/10/01"},"accession":"GSE335399","cross_references":{"GSM":["GSM9812864","GSM9812863","GSM9812866","GSM9812865","GSM9812860","GSM9812870","GSM9812862","GSM9812861","GSM9812868","GSM9812867","GSM9812859","GSM9812869"],"GPL":["11154"],"GSE":["335399"],"taxon":["Homo sapiens"]}}