Genetic manipulation of LKB1 elicits lethal metastatic prostate cancer
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F20%3A10410893" target="_blank" >RIV/00216208:11130/20:10410893 - isvavai.cz</a>
Alternative codes found
RIV/00064203:_____/20:10410893
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=vC4Fv79BH8" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=vC4Fv79BH8</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1084/jem.20191787" target="_blank" >10.1084/jem.20191787</a>
Alternative languages
Result language
angličtina
Original language name
Genetic manipulation of LKB1 elicits lethal metastatic prostate cancer
Original language description
Gene dosage is a key defining factor to understand cancer pathogenesis and progression, which requires the development of experimental models that aid better deconstruction of the disease. Here, we model an aggressive form of prostate cancer and show the unconventional association of LKB1 dosage to prostate tumorigenesis. Whereas loss of Lkb1 alone in the murine prostate epithelium was inconsequential for tumorigenesis, its combination with an oncogenic insult, illustrated by Pten heterozygosity, elicited lethal metastatic prostate cancer. Despite the low frequency of LKB1 deletion in patients, this event was significantly enriched in lung metastasis. Modeling the role of LKB1 in cellular systems revealed that the residual activity retained in a reported kinase-dead form, LKB1K78I, was sufficient to hamper tumor aggressiveness and metastatic dissemination. Our data suggest that prostate cells can function normally with low activity of LKB1, whereas its complete absence influences prostate cancer pathogenesis and dissemination. (C) 2020 Hermanova et al.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30204 - Oncology
Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2020
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Journal of Experimental Medicine
ISSN
0022-1007
e-ISSN
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Volume of the periodical
217
Issue of the periodical within the volume
6
Country of publishing house
US - UNITED STATES
Number of pages
19
Pages from-to
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UT code for WoS article
000538138000011
EID of the result in the Scopus database
2-s2.0-85082561362