Targeting endoplasmic reticulum signaling pathways in cancer.
The endoplasmic reticulum (ER) orchestrates the production of membrane-bound and secreted proteins. However, its capacity to process the synthesis and folding of protein is limited. Protein overload and the accumulation of misfolded proteins in the ER trigger an adaptive response known as the ER-stress response that is mediated by specific ER-anchored signaling pathways. This response regulates cell functions aimed at restoring cellular homeostasis or at promoting apoptosis of irreparably damaged cells. Activation or deregulation of ER-signaling pathways has been associated with various diseases including cancer. Here we discuss how tumors engage ER-signaling pathways to promote tumorigenesis and how manipulation of this process by anticancer drugs may contribute to cancer treatment.
Department of Biochemistry, University of Lausanne, 155 Ch. Des Boveresses, Epalinges 1066, Switzerland.
Fabio
F
Martinon
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D001897:Boronic Acids / Q000494:pharmacology; D000069286:Bortezomib; D004721:Endoplasmic Reticulum / Q000187:drug effects* / Q000378:metabolism*; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects; D017320:HIV Protease Inhibitors / Q000494:pharmacology; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy* / Q000378:metabolism*; D046988:Proteasome Endopeptidase Complex / Q000187:drug effects; D017510:Protein Folding / Q000187:drug effects; D011719:Pyrazines / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects*
D000970:Antineoplastic Agents; D001897:Boronic Acids; D017320:HIV Protease Inhibitors; D011719:Pyrazines; D000069286:Bortezomib; D046988:Proteasome Endopeptidase Complex