Homeostatic interplay between FoxO proteins and ER proteostasis in cancer and other diseases
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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.
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
Artículo de publicación ISI
Quote ItemSeminars in Cancer Biology Volumen: 50 Páginas: 42-52
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