{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE341nnn/GSE341921/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE341921"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"PGK1 moonlights as an NF-kB/p65 kinase to orchestrate M2-like macrophage-mediated immunosuppression in triple-negative breast cancer","description":"Triple-negative breast cancer (TNBC) is the most aggressive molecular subtype with limited therapeutic options. Metabolic reprogramming is a hallmark of cancer, and emerging evidence indicates metabolic enzymes possess non-canonical moonlighting functions. We identified phosphoglycerate kinase 1 (PGK1) as a key link between glycolysis and immunosuppression in TNBC. To investigate the role of PGK1 in shaping the tumor immune microenvironment, we performed single-cell RNA sequencing (scRNA-seq) on TNBC cells (4T1) with PGK1 knockdown (shPgk1) and negative control (shNC), each with three biological replicates. Single-cell libraries were prepared on the TaiM4 scRNA platform and sequenced on the BGI DNBSEQ platform using paired-end sequencing. A total of 33,138 high-quality cells were retained after quality filtering. Our analysis revealed that PGK1 knockdown significantly altered the transcriptional landscape and immune signaling pathways in TNBC cells.","dates":{"publication":"2026/08/06"},"accession":"GSE341921","cross_references":{"GSM":["GSM9920066","GSM9920065","GSM9920064","GSM9920063","GSM9920062","GSM9920061"],"GPL":["28457"],"GSE":["341921"],"taxon":["Mus musculus"]}}