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@ARTICLE{Catanzaro:141996,
      author       = {G. Catanzaro and Z. M. Besharat and E. Miele and M.
                      Chiacchiarini and A. Po and A. Carai and C. E. Marras and M.
                      Antonelli and M. Badiali and A. Raso and S. Mascelli and D.
                      Schrimpf$^*$ and D. Stichel$^*$ and M. Tartaglia and D.
                      Capper$^*$ and A. von Deimling$^*$ and F. Giangaspero and A.
                      Mastronuzzi and F. Locatelli and E. Ferretti},
      title        = {{T}he mi{R}-139-5p regulates proliferation of
                      supratentorial paediatric low-grade gliomas by targeting the
                      {PI}3{K}/{AKT}/m{TORC}1 signalling.},
      journal      = {Neuropathology $\&$ applied neurobiology},
      volume       = {44},
      number       = {7},
      issn         = {0305-1846},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DKFZ-2018-02226},
      pages        = {687 - 706},
      year         = {2018},
      abstract     = {Paediatric low-grade gliomas (pLGGs) are a heterogeneous
                      group of brain tumours associated with a high overall
                      survival: however, they are prone to recur and
                      supratentorial lesions are difficult to resect, being
                      associated with high percentage of disease recurrence. Our
                      aim was to shed light on the biology of pLGGs.We performed
                      microRNA profiling on 45 fresh-frozen grade I tumour samples
                      of various histological classes, resected from patients aged
                      ≤16 years. We identified 93 microRNAs specifically
                      dysregulated in tumours as compared to non-neoplastic brain
                      tissue. Pathway analysis of the microRNAs signature revealed
                      PI3K/AKT signalling as one of the centrally enriched
                      oncogenic signalling. To date, activation of the PI3K/AKT
                      pathway in pLGGs has been reported, although activation
                      mechanisms have not been fully investigated yet.One of the
                      most markedly down-regulated microRNAs in our supratentorial
                      pLGGs cohort was miR-139-5p, whose targets include the gene
                      encoding the PI3K's (phosphatidylinositol 3-kinase)
                      catalytic unit, PIK3CA. We investigated the role of
                      miR-139-5p in regulating PI3K/AKT signalling by the use of
                      human cell cultures derived from supratentorial pLGGs.
                      MiR-139-5p overexpression inhibited pLGG cell proliferation
                      and decreased the phosphorylation of PI3K target AKT and
                      phosphorylated-p70 S6 kinase (p-p70 S6K), a hallmark of
                      PI3K/AKT/mTORC1 signalling activation. The effect of
                      miR-139-5p was mediated by PI3K inhibition, as suggested by
                      the decrease in proliferation and phosphorylation of AKT and
                      p70 S6K after treatment with the direct PI3K inhibitor
                      LY294002.These findings provide the first evidence that
                      down-regulation of miR-139-5p in supratentorial pLGG drives
                      cell proliferation by derepressing PI3K/AKT signalling.},
      cin          = {L201 / G380},
      ddc          = {610},
      cid          = {I:(DE-He78)L201-20160331 / I:(DE-He78)G380-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29478280},
      doi          = {10.1111/nan.12479},
      url          = {https://inrepo02.dkfz.de/record/141996},
}