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@ARTICLE{Drula:276347,
      author       = {R. Drula and B. Pardini and X. Fu and M. C. De Los Santos
                      and A. Jurj and L. Pang and S. M. El-Daly and L. Fabris and
                      E. Knutsen and M.-P. Dragomir$^*$ and R. Bayraktar and Y. Li
                      and M. Chen and F. Del Vecchio and L. Berland and J. Dae and
                      D. Fan and M. Shimizu and A. M. Tran and M. Barzi and C.
                      Pioppini and A. M. Gutierrez and C. Ivan and S. Meas and C.
                      S. Hall and S. K. Alahari and I. Berindan-Neagoe and M.
                      Fabbri and A. Lucci and B. Arun and S. Anfossi and G. A.
                      Calin},
      title        = {17β-estradiol promotes extracellular vesicle release and
                      selective mi{RNA} loading in {ER}α-positive breast cancer.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {120},
      number       = {23},
      issn         = {0027-8424},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DKFZ-2023-01067},
      pages        = {e2122053120},
      year         = {2023},
      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-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.},
      keywords     = {breast cancer (Other) / estrogen receptor (Other) /
                      exosomes (Other) / extracellular vesicles (Other) /
                      microRNAs (Other)},
      cin          = {BE01},
      ddc          = {500},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37252969},
      doi          = {10.1073/pnas.2122053120},
      url          = {https://inrepo02.dkfz.de/record/276347},
}