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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-7d-5p in EVs derived from the blood of premenopausal ER+ BC patients, and elevated EV levels in patients with high BMI, both conditions associated with higher levels of 17β-estradiol. In brief, we identified a unique estrogen-driven mechanism by which ER+ BC cells eliminate tumor suppressor miRNAs in EVs, with effects on modulating tumor-associated macrophages in the microenvironment.

Titel:	17β-estradiol promotes extracellular vesicle release and selective miRNA loading in ERα-positive breast cancer.
Autor/in / Beteiligte Person:	Drula, R ; Pardini, B ; Fu, X ; De Los Santos, MC ; Jurj, A ; Pang, L ; El-Daly, SM ; Fabris, L ; Knutsen, E ; Dragomir, MP ; Bayraktar, R ; Li, Y ; Chen, M ; Del Vecchio, F ; Berland, L ; Dae, J ; Fan, D ; Shimizu, M ; Tran, AM ; Barzi, M ; Pioppini, C ; Gutierrez, AM ; Ivan, C ; Meas, S ; Hall, CS ; Alahari, SK ; Berindan-Neagoe, I ; Fabbri, M ; Lucci, A ; Arun, B ; Anfossi, S ; Calin, GA
Link:	Full Text Finder (Volltext)
Zeitschrift:	Proceedings of the National Academy of Sciences of the United States of America, Jg. 120 (2023-06-06), Heft 23, S. e2122053120
Veröffentlichung:	Washington, DC : National Academy of Sciences, 2023
Medientyp:	academicJournal
ISSN:	1091-6490 (electronic)
DOI:	10.1073/pnas.2122053120
Schlagwort:	Humans Female Estrogen Receptor alpha genetics Estrogen Receptor alpha metabolism Estradiol pharmacology Estradiol metabolism Estrogens metabolism Tumor Microenvironment MicroRNAs genetics MicroRNAs metabolism Breast Neoplasms pathology Extracellular Vesicles genetics Extracellular Vesicles metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Language: English [Proc Natl Acad Sci U S A] 2023 Jun 06; Vol. 120 (23), pp. e2122053120. <i>Date of Electronic Publication: </i>2023 May 30. MeSH Terms: MicroRNAs* / genetics ; MicroRNAs* / metabolism ; Breast Neoplasms* / pathology ; Extracellular Vesicles* / genetics ; Extracellular Vesicles* / metabolism ; Humans ; Female ; Estrogen Receptor alpha / genetics ; Estrogen Receptor alpha / metabolism ; Estradiol / pharmacology ; Estradiol / metabolism ; Estrogens / metabolism ; Tumor Microenvironment References: Int J Mol Sci. 2016 Dec 02;17(12):. (PMID: 27918449) ; Clin Cancer Res. 2013 Dec 1;19(23):6389-97. (PMID: 24298069) ; Cell. 2010 Oct 1;143(1):46-58. (PMID: 20887892) ; Trends Endocrinol Metab. 2012 Feb;23(2):73-82. (PMID: 22257677) ; Br J Cancer. 2019 Feb;120(3):331-339. 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(PMID: 31899528) Grant Information: R01 CA222007 United States CA NCI NIH HHS; R01 CA219024 United States CA NCI NIH HHS; R01 GM122775 United States GM NIGMS NIH HHS; R01 CA182905 United States CA NCI NIH HHS; P50 CA127001 United States CA NCI NIH HHS; R01 CA215753 United States CA NCI NIH HHS Contributed Indexing: Keywords: breast cancer; estrogen receptor; exosomes; extracellular vesicles; microRNAs Substance Nomenclature: 0 (MicroRNAs) ; 0 (Estrogen Receptor alpha) ; 4TI98Z838E (Estradiol) ; 0 (Estrogens) ; 0 (MIRN149 microRNA, human) Entry Date(s): Date Created: 20230530 Date Completed: 20230601 Latest Revision: 20231201 Update Code: 20240514 PubMed Central ID: PMC10266002

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17β-estradiol promotes extracellular vesicle release and selective miRNA loading in ERα-positive breast cancer.