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@ARTICLE{Miele:163162,
      author       = {E. Miele and A. Po and A. Mastronuzzi and A. Carai and Z.
                      M. Besharat and N. Pediconi and L. Abballe and G. Catanzaro
                      and C. Sabato and E. De Smaele and G. Canettieri and L. Di
                      Marcotullio and A. Vacca and A. Mai and M. Levrero and S. M.
                      Pfister$^*$ and M. Kool$^*$ and F. Giangaspero and F.
                      Locatelli and E. Ferretti},
      title        = {{D}ownregulation of mi{R}-326 and its host gene
                      β-arrestin1 induces pro survival activity of {E}2{F}1 and
                      promotes medulloblastoma growth.},
      journal      = {Molecular oncology},
      volume       = {15},
      number       = {2},
      issn         = {1574-7891},
      address      = {Hoboken, NJ},
      publisher    = {John Wiley $\&$ Sons, Inc.},
      reportid     = {DKFZ-2020-01865},
      pages        = {523-542},
      year         = {2021},
      note         = {2021 Feb;15(2):523-542},
      abstract     = {Persistent mortality rates of medulloblastoma (MB) and
                      severe side effects of the current therapies require the
                      definition of the molecular mechanisms that contribute to
                      tumor progression. Using cultured MB cancer stem cells and
                      xenograft tumors generated in mice, we show that low
                      expression of miR-326 and its host gene β-arrestin1 (ARRB1)
                      promotes tumor growth enhancing the E2F1 pro-survival
                      function. Our models revealed that miR-326 and ARRB1 are
                      controlled by a bivalent domain, since the H3K27me3
                      repressive mark is found at their regulatory region together
                      with the activation-associated H3K4me3 mark. High levels of
                      EZH2, a feature of MB, are responsible for the presence of
                      H3K27me3. Ectopic expression of miR-326 and ARRB1 provides
                      hints into how their low levels regulate E2F1 activity.
                      MiR-326 targets E2F1 mRNA, thereby reducing its protein
                      levels; ARRB1, triggering E2F1 acetylation, reverses its
                      function into pro-apoptotic activity. Similar to miR-326 and
                      ARRB1 overexpression, we also show that EZH2 inhibition
                      restores miR-326/ARRB1 expression, limiting E2F1
                      pro-proliferative activity. Our results reveal a new
                      regulatory molecular axis critical for MB progression.},
      cin          = {B062},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32920979},
      doi          = {10.1002/1878-0261.12800.},
      url          = {https://inrepo02.dkfz.de/record/163162},
}