Homeostatic interplay between FoxO proteins and ER proteostasis in cancer and other diseases
Author
dc.contributor.author
González Quiroz, Matias
Author
dc.contributor.author
Urra, Hery
Author
dc.contributor.author
Limia, Celia María
Author
dc.contributor.author
Hetz Flores, Claudio
Admission date
dc.date.accessioned
2018-11-08T20:21:19Z
Available date
dc.date.available
2018-11-08T20:21:19Z
Publication date
dc.date.issued
2018-06
Cita de ítem
dc.identifier.citation
Seminars in Cancer Biology Volumen: 50 Páginas: 42-52
es_ES
Identifier
dc.identifier.other
10.1016/j.semcancer.2018.01.011
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/152515
Abstract
dc.description.abstract
Cancer cells are exposed to adverse conditions within the tumor microenvironment that challenge cells to adapt and survive. Several of these homeostatic perturbations insults alter the normal function of the endoplasmic reticulum (ER), resulting in the accumulation of misfolded proteins. ER stress triggers a conserved signaling pathway known as the unfolded protein response (UPR) to cope with the stress or trigger apoptosis of damaged cells. The UPR has been described as a major driver in the acquisition of malignant characteristics that ultimately lead to cancer progression. Although, several reports describe the relevance of the UPR in tumor growth, the possible crosstalk with other cancer-related pathways is starting to be elucidated. The Forkhead Box O (FoxO) subfamily of proteins has a major role in cancer progression, where chromosomal translocations and deregulated signaling lead to loss-of-function of FoxO proteins, contributing to tumor progression. Here we discuss the homeostatic connection between the UPR and FoxO proteins and its possible implications to tumor progression and the acquisition of several hallmarks of cancer. In addition, studies linking a crosstalk between the UPR and FoxO proteins in other diseases, including neurodegeneration and metabolic disorders is provided.
es_ES
Patrocinador
dc.description.sponsorship
FONDECYT
1140549
3160461
Millennium Institute
P09-015-F
FONDAP15150012
BNI
European Commission RD MSCA-RISE
734749
US Office of Naval Research Global
(ONR-G)N62909-16-1-2003
U.S. Air Force Office of Scientific Research
FA9550-16-1-0384
CONICYT-Brazil
441921/2016-7
CONICYT fellowship
CONICYT-PCHA/Doctorado Nacional/2016-21160232
CONICYT-PCHA/Doctorado Nacional/2016-21160967
CONICYT research grant
FONDEFID16I10223
FONDEFD11E1007