2024-03-29T09:09:47Zhttp://repisalud.isciii.es/oai/requestoai:repisalud.isciii.es:20.500.12105/73492023-10-17T07:37:18Zcom_20.500.12105_2152com_20.500.12105_2051com_20.500.12105_2144com_20.500.12105_2145col_20.500.12105_2153col_20.500.12105_2146
Repisalud
author
Quirós, Pedro M
author
Español, Yaiza
author
Acin-Perez, Rebeca
author
Rodríguez, Francisco
author
Bárcena, Clea
author
Watanabe, Kenta
author
Calvo, Enrique
author
Loureiro, Marta
author
Fernández-García, M Soledad
author
Fueyo, Antonio
author
Vazquez, Jesus
author
Enriquez, Jose Antonio
author
López-Otín, Carlos
funder
Ministerio de Economía y Competitividad (España)
funder
Instituto de Salud Carlos III
funder
Redes Temáticas de Investigación Cooperativa en Salud (RETICS) (España)
funder
Fundación Cajastur
funder
Japan Society for the Promotion of Science (Japón)
funder
Botín Foundation
2019-03-18T09:54:00Z
2019-03-18T09:54:00Z
2014-07-24
Cell Rep. 2014; 8(2):542-56
22111247
http://hdl.handle.net/20.500.12105/7349
25017063
10.1016/j.celrep.2014.06.018
2211-1247
Cell reports
We generated mice deficient in Lon protease (LONP1), a major enzyme of the mitochondrial quality control machinery. Homozygous deletion of Lonp1 causes early embryonic lethality, whereas its haploinsufficiency protects against colorectal and skin tumors. Furthermore, LONP1 knockdown inhibits cellular proliferation and tumor and metastasis formation, whereas its overexpression increases tumorigenesis. Clinical studies indicate that high levels of LONP1 are a poor prognosis marker in human colorectal cancer and melanoma. Additionally, functional analyses show that LONP1 plays a key role in metabolic reprogramming by remodeling OXPHOS complexes and protecting against senescence. Our findings demonstrate the relevance of LONP1 for cellular and organismal viability and identify this protease as a central regulator of mitochondrial activity in oncogenesis.
eng
ATP-dependent Lon protease controls tumor bioenergetics by reprogramming mitochondrial activity
journal article
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