{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339083/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Non-coding RNA profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE339083"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Effect of TENT2 knockdown on miRNA profiling in human lung endothelial cells","description":"MiRNAs are generated through a finely tuned multi-step process that includes precise cropping and cleavage of their precursors. The mature miRNA is then loaded onto an argonaute (Ago) protein to form an RNA-induced silencing complex (RISC) and target messenger RNAs. Most of the mechanisms of miRNA regulation target one of the steps in the biogenesis. However, through analysis of miR-1 precursors, we demonstrate that VEGF stimulation induces degradation (decay) of mature miR-1-3p without affecting its precursors. This analysis also identified a specific miRNA 3’-adenylation pathway that targets the guide strand after RISC loading. VEGF induced the expression of terminal nucleotidyl transferase 2 (TENT2, also known as PAPD4 or GLD2), one of the main enzymes that mediate 3’ miRNA adenylation, and knockdown of TENT2 inhibited miR-1 decay. We examined the biological significance of TENT2 in VEGF-mediated EC proliferation, its pathogenic role in murine NSCLC models, and its expression and clinical significance in human NSCLC.","dates":{"publication":"2026/07/22"},"accession":"GSE339083","cross_references":{"GSM":["GSM9888182","GSM9888185","GSM9888186","GSM9888183","GSM9888184","GSM9888187"],"GPL":["34281"],"GSE":["339083"],"taxon":["Homo sapiens"]}}