{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Drula R"],"funding":["NCI NIH HHS","NIGMS NIH HHS"],"pagination":["e2122053120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10266002"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(23)"],"pubmed_abstract":["The causes and consequences of abnormal biogenesis of extracellular vesicles (EVs) are not yet well understood in malignancies, including in breast cancers (BCs). Given the hormonal signaling dependence of estrogen receptor-positive (ER+) BC, we hypothesized that 17β-estradiol (estrogen) might influence EV production and microRNA (miRNA) loading. We report that physiological doses of 17β-estradiol promote EV secretion specifically from ER+ BC cells via inhibition of miR-149-5p, hindering its regulatory activity on SP1, a transcription factor that regulates the EV biogenesis factor nSMase2. Additionally, miR-149-5p downregulation promotes hnRNPA1 expression, responsible for the loading of let-7's miRNAs into EVs. In multiple patient cohorts, we observed increased levels of let-7a-5p and let"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["17β-estradiol promotes extracellular vesicle release and selective miRNA loading in ERα-positive breast cancer."],"pmcid":["PMC10266002"],"funding_grant_id":["R01 CA222007","P50 CA127001","R01 GM122775","R01 CA219024","R01 CA215753","R01 CA182905"],"pubmed_authors":["Fabris L","Shimizu M","Dragomir MP","Lucci A","Fu X","Berindan-Neagoe I","Alahari SK","Berland L","Fabbri M","El-Daly SM","Fan D","Knutsen E","Ivan C","Arun B","Gutierrez AM","Chen M","Jurj A","Pioppini C","Barzi M","Li Y","Del Vecchio F","Anfossi S","Calin GA","Pang L","Pardini B","Dae J","Tran AM","Drula R","De Los Santos MC","Hall CS","Bayraktar R","Meas S"],"additional_accession":[]},"is_claimable":false,"name":"17β-estradiol promotes extracellular vesicle release and selective miRNA loading in ERα-positive breast cancer.","description":"The causes and consequences of abnormal biogenesis of extracellular vesicles (EVs) are not yet well understood in malignancies, including in breast cancers (BCs). Given the hormonal signaling dependence of estrogen receptor-positive (ER+) BC, we hypothesized that 17β-estradiol (estrogen) might influence EV production and microRNA (miRNA) loading. We report that physiological doses of 17β-estradiol promote EV secretion specifically from ER+ BC cells via inhibition of miR-149-5p, hindering its regulatory activity on SP1, a transcription factor that regulates the EV biogenesis factor nSMase2. Additionally, miR-149-5p downregulation promotes hnRNPA1 expression, responsible for the loading of let-7's miRNAs into EVs. In multiple patient cohorts, we observed increased levels of let-7a-5p and let","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jun","modification":"2026-04-29T02:21:39.796Z","creation":"2025-02-19T01:18:58.345Z"},"accession":"S-EPMC10266002","cross_references":{"pubmed":["37252969"],"doi":["10.1073/pnas.2122053120"]}}