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@ARTICLE{Proestler:282915,
      author       = {E. Proestler and J. Donzelli and S. Nevermann and K.
                      Breitwieser and L. F. Koch and T. Best and M. Fauth and M.
                      Wickström and P. Harter$^*$ and P. Kogner and G. Lavieu and
                      K. Larsson and M. J. Saul},
      title        = {{T}he multiple functions of mi{R}-574-5p in the
                      neuroblastoma tumor microenvironment.},
      journal      = {Frontiers in pharmacology},
      volume       = {14},
      issn         = {1663-9812},
      address      = {Lausanne},
      publisher    = {Frontiers Media},
      reportid     = {DKFZ-2023-01904},
      pages        = {1183720},
      year         = {2023},
      abstract     = {Neuroblastoma is the most common extracranial solid tumor
                      in childhood and arises from neural crest cells of the
                      developing sympathetic nervous system. Prostaglandin E2
                      (PGE2) has been identified as a key pro-inflammatory
                      mediator of the tumor microenvironment (TME) that promotes
                      neuroblastoma progression. We report that the interaction
                      between the microRNA miR-574-5p and CUG-binding protein 1
                      (CUGBP1) induces the expression of microsomal prostaglandin
                      E2 synthase 1 (mPGES-1) in neuroblastoma cells, which
                      contributes to PGE2 biosynthesis. PGE2 in turn specifically
                      induces the sorting of miR-574-5p into small extracellular
                      vesicles (sEV) in neuroblastoma cell lines. sEV are one of
                      the major players in intercellular communication in the TME.
                      We found that sEV-derived miR-574-5p has a paracrine
                      function in neuroblastoma. It acts as a direct Toll-like
                      receptor 7/8 (TLR7/8) ligand and induces α-smooth muscle
                      actin (α-SMA) expression in fibroblasts, contributing to
                      fibroblast differentiation. This is particularly noteworthy
                      as it has an opposite function to that in the TME of lung
                      carcinoma, another PGE2 dependent tumor type. Here,
                      sEV-derived miR-574-5p has an autokrine function that
                      inhibits PGE2 biosynthesis in lung cancer cells. We report
                      that the tetraspanin composition on the surface of sEV is
                      associated with the function of sEV-derived miR-574-5p. This
                      suggests that the vesicles do not only transport miRs, but
                      also appear to influence their mode of action.},
      keywords     = {NSCLC (Other) / PGE2 (Other) / TLR7/8 (Other) / miR-574-5p
                      (Other) / neuroblastoma (Other) / tetraspanins (Other)},
      cin          = {FM01},
      ddc          = {610},
      cid          = {I:(DE-He78)FM01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37731742},
      pmc          = {pmc:PMC10507178},
      doi          = {10.3389/fphar.2023.1183720},
      url          = {https://inrepo02.dkfz.de/record/282915},
}