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M609267200v1
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Papers In Press, published online ahead of print November 29, 2006
J. Biol. Chem, 10.1074/jbc.M609267200
Submitted on September 29, 2006
Revised on November 28, 2006
Accepted on November 29, 2006

Differential effects of endoplasmic reticulum stress-induced autophagy on cell survival

Wen-Xing Ding, Hong-Min Ni, Wentao Gao, Yi-Feng Hou, Melissa A. Melan, Xiaoyun Chen, Donna B. Stolz, Zhi-Ming Shao, and Xiao-Ming Yin

Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261

Corresponding Author: xmyin{at}pitt.edu

Autophagy is a cellular response to adverse environment and stress but its significance in cell survival is not always clear. Here we show that autophagy could be induced in the mammalian cells by chemicals, such as A23187, tunicamycin, thapsigargin and brefeldin A, that cause endoplasmic reticulum stress. Endoplasmic reticulum stress-induced autophagy is important for clearing poly-ubiquitinated protein aggregates and for reducing cellular vacuolization in HCT116 colon cancer cells and DU145 prostate cancer cells, thus mitigating endoplasmic reticulum stress and protecting against cell death. In contrast, autophagy induced by the same chemicals does not confer protection in a normal human colon cell line and in the non-transformed murine embryonic fibroblasts, but rather contributes to cell death. Thus the impact of autophagy on cell survival during endoplasmic reticulum stress is likely contingent on the status of cells, which could be explored for tumor-specific therapy.


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