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©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Biol Chem. Oct 26, 2011; 2(10): 226-231
Published online Oct 26, 2011. doi: 10.4331/wjbc.v2.i10.226
Published online Oct 26, 2011. doi: 10.4331/wjbc.v2.i10.226
Survival and death of endoplasmic-reticulum-stressed cells: Role of autophagy
Yan Cheng, Jin-Ming Yang, Department of Pharmacology and Penn State Hershey Cancer Institute, The Pennsylvania State University College of Medicine, Hershey, PA 17033-0850, United States
Author contributions: Cheng Y and Yang JM wrote the review together.
Supported by Grants from the US Public Health Service R01CA135038 (Yang JM), and from the Department of Defense BC103654 (Cheng Y)
Correspondence to: Jin-Ming Yang, MD, PhD, Department of Pharmacology and Penn State Hershey Cancer Institute, The Pennsylvania State University College of Medicine, CH74, 500 University Drive, PO Box 850, Hershey, PA 17033-0850, United States. juy16@psu.edu
Telephone: +1-717-5311630 Fax: +1-717-5310011
Received: July 7, 2011
Revised: September 3, 2011
Accepted: September 10, 2011
Published online: October 26, 2011
Revised: September 3, 2011
Accepted: September 10, 2011
Published online: October 26, 2011
Abstract
Accumulation of unfolded proteins in the endoplasmic reticulum (ER) results in ER stress, which subsequently activates the unfolded protein response that induces a transcriptional program to alleviate the stress. Another cellular process that is activated during ER stress is autophagy, a mechanism of enclosing intracellular components in a double-membrane autophagosome, and then delivering it to the lysosome for degradation. Here, we discuss the role of autophagy in cellular response to ER stress, the signaling pathways linking ER stress to autophagy, and the possible implication of modulating autophagy in treatment of diseases such as cancer.
Keywords: Endoplasmic reticulum stress, Autophagy, Apoptosis, Cell survival, Cell death