Unfolded protein response to autophagy as a promising druggable target for anticancer therapy
Identifieur interne : 001322 ( Main/Exploration ); précédent : 001321; suivant : 001323Unfolded protein response to autophagy as a promising druggable target for anticancer therapy
Auteurs : Dong Hoon Suh [Corée du Sud] ; Mi-Kyung Kim [Corée du Sud] ; Hee Seung Kim [Corée du Sud] ; Hyun Hoon Chung [Corée du Sud] ; Yong Sang Song [Corée du Sud]Source :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2012-10.
English descriptors
- Teeft :
- Acad, Anticancer, Apoptosis, Apoptotic, Atf4, Atf6, Autophagic cell death, Autophagosome formation, Autophagy, Autophagy inhibition, Beclin1, Biol, Bortezomib, Cancer biol, Cancer cells, Carcinoma, Cell death, Cell survival, Cellular stress responses, Deacetylase, Endoplasmic, Endoplasmic reticulum, Endoplasmic reticulum stress, Glucose deprivation, Hdac, Hdac inhibitors, Heat shock protein, Histone, Inducer, Inhibitor, Intrinsic pathway, Ire1, Kinase, Lymphoma, Mammalian target, Misfolded proteins, Mtor, Myeloma, Nature reviews, Normal cells, Pancreatic, Pathway, Perk, Phosphorylation, Prostate, Protease, Protease inhibitors, Proteasome, Proteasome inhibitors, Protein response, Protein synthesis, Reticulum, Seoul, Stress response, Stress response pathways, Stress responses, Tumor cells, Tumor growth, Xbp1, York academy.
Abstract
The endoplasmic reticulum (ER) is responsible for protein processing. In rapidly proliferating tumor cells, the ER tends to be overloaded with unfolded and misfolded proteins due to high metabolic demand. With the limited protein‐folding capacity of the ER, tumor cells often suffer from more ER stress than do normal cells. Thus, cellular stress responses to cope with ER stress, such as the unfolded protein response (UPR) and autophagy, might be more activated in cancer cells than in normal cells. The complex signaling pathways from the UPR to autophagy provide promising druggable targets; a number of UPR/autophagy‐targeted anticancer agents are currently in development in preclinical and clinical studies. In this short review we will discuss the potential anticancer efficacy of modulators of cellular stress responses, especially UPR and autophagy, on the basis of their signaling pathways. In addition, the current developmental status of the UPR/autophagy‐targeted agents will be discussed.
Url:
DOI: 10.1111/j.1749-6632.2012.06739.x
Affiliations:
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cells</term><term>Pancreatic</term><term>Pathway</term><term>Perk</term><term>Phosphorylation</term><term>Prostate</term><term>Protease</term><term>Protease inhibitors</term><term>Proteasome</term><term>Proteasome inhibitors</term><term>Protein response</term><term>Protein synthesis</term><term>Reticulum</term><term>Seoul</term><term>Stress response</term><term>Stress response pathways</term><term>Stress responses</term><term>Tumor cells</term><term>Tumor growth</term><term>Xbp1</term><term>York academy</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The endoplasmic reticulum (ER) is responsible for protein processing. 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