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@ARTICLE{Moussa:294358,
author = {A. Moussa$^*$ and M. R. Cosenza$^*$ and T. Wohlfromm$^*$
and K. Brobeil$^*$ and A. Hill$^*$ and A. Patrizi$^*$ and K.
Müller-Decker$^*$ and T. Holland-Letz$^*$ and A. Jauch and
B. Kraft$^*$ and A. Krämer$^*$},
title = {{STIL} overexpression shortens lifespan and reduces tumor
formation in mice.},
journal = {PLoS Genetics},
volume = {20},
number = {10},
issn = {1553-7390},
address = {San Francisco, Calif.},
publisher = {Public Library of Science},
reportid = {DKFZ-2024-02191},
pages = {e1011460 -},
year = {2024},
note = {#EA:A360#LA:A360#},
abstract = {Centrosomes are the major microtubule organizing centers of
animal cells. Supernumerary centrosomes are a common feature
of human tumors and associated with karyotype abnormalities
and aggressive disease, but whether they are cause or
consequence of cancer remains controversial. Here, we
analyzed the consequences of centrosome amplification by
generating transgenic mice in which centrosome numbers can
be increased by overexpression of the structural centrosome
protein STIL. We show that STIL overexpression induces
centrosome amplification and aneuploidy, leading to
senescence, apoptosis, and impaired proliferation in mouse
embryonic fibroblasts, and microcephaly with increased
perinatal lethality and shortened lifespan in mice.
Importantly, both overall tumor formation in mice with
constitutive, global STIL overexpression and chemical skin
carcinogenesis in animals with inducible, skin-specific STIL
overexpression were reduced, an effect that was not rescued
by concomitant interference with p53 function. These results
suggest that supernumerary centrosomes impair proliferation
in vitro as well as in vivo, resulting in reduced lifespan
and delayed spontaneous as well as carcinogen-induced tumor
formation.},
cin = {A360 / A320 / W420 / C060},
ddc = {610},
cid = {I:(DE-He78)A360-20160331 / I:(DE-He78)A320-20160331 /
I:(DE-He78)W420-20160331 / I:(DE-He78)C060-20160331},
pnm = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
pid = {G:(DE-HGF)POF4-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:39466849},
doi = {10.1371/journal.pgen.1011460},
url = {https://inrepo02.dkfz.de/record/294358},
}