% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@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},
}