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@ARTICLE{Bartl:909166,
      author       = {Bartl, Jasmin and Zanini, Marco and Bernardi, Flavia and
                      Forget, Antoine and Blümel, Lena and Talbot, Julie and
                      Picard, Daniel and Qin, Nan and Cancila, Gabriele and Gao,
                      Qingsong and Nath, Soumav and Koumba, Idriss Mahoungou and
                      Wolter, Marietta and Kuonen, François and Langini, Maike
                      and Beez, Thomas and Munoz, Christopher and Pauck, David and
                      Marquardt, Viktoria and Yu, Hua and Souphron, Judith and
                      Korsch, Mascha and Mölders, Christina and Berger, Daniel
                      and Göbbels, Sarah and Meyer, Frauke-Dorothee and
                      Scheffler, Björn and Rotblat, Barak and Diederichs, Sven
                      and Ramaswamy, Vijay and Suzuki, Hiromishi and Oro, Anthony
                      and Stühler, Kai and Stefanski, Anja and Fischer, Ute and
                      Leprivier, Gabriel and Willbold, Dieter and Steger, Gerhard
                      and Buell, Alexander and Kool, Marcel and Lichter, Peter and
                      Pfister, Stefan M. and Northcott, Paul A. and Taylor,
                      Michael D. and Borkhardt, Arndt and Reifenberger, Guido and
                      Ayrault, Olivier and Remke, Marc},
      title        = {{T}he {HHIP}-{AS}1 lnc{RNA} promotes tumorigenicity through
                      stabilization of dynein complex 1 in human {SHH}-driven
                      tumors},
      journal      = {Nature Communications},
      volume       = {13},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {FZJ-2022-03044},
      pages        = {4061},
      year         = {2022},
      abstract     = {Most lncRNAs display species-specific expression patterns
                      suggesting that animal models of cancer may only
                      incompletely recapitulate the regulatory crosstalk between
                      lncRNAs and oncogenic pathways in humans. Among these
                      pathways, Sonic Hedgehog (SHH) signaling is aberrantly
                      activated in several human cancer entities. We unravel that
                      aberrant expression of the primate-specific lncRNA HedgeHog
                      Interacting Protein-AntiSense 1 (HHIP-AS1) is a hallmark of
                      SHH-driven tumors including medulloblastoma and atypical
                      teratoid/rhabdoid tumors. HHIP-AS1 is actively transcribed
                      from a bidirectional promoter shared with SHH regulator
                      HHIP. Knockdown of HHIP-AS1 induces mitotic spindle
                      deregulation impairing tumorigenicity in vitro and in vivo.
                      Mechanistically, HHIP-AS1 binds directly to the mRNA of
                      cytoplasmic dynein 1 intermediate chain 2 (DYNC1I2) and
                      attenuates its degradation by hsa-miR-425-5p. We uncover
                      that neither HHIP-AS1 nor the corresponding regulatory
                      element in DYNC1I2 are evolutionary conserved in mice. Taken
                      together, we discover an lncRNA-mediated mechanism that
                      enables the pro-mitotic effects of SHH pathway activation in
                      human tumors.},
      cin          = {IBI-7},
      ddc          = {500},
      cid          = {I:(DE-Juel1)IBI-7-20200312},
      pnm          = {5244 - Information Processing in Neuronal Networks
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {35831316},
      UT           = {WOS:000825090700001},
      doi          = {10.1038/s41467-022-31574-z},
      url          = {https://juser.fz-juelich.de/record/909166},
}