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, Xiao Ming Yin

Research output: Contribution to journalArticle

366 Scopus citations

Abstract

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 polyubiquitinated 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.

Original languageEnglish (US)
Pages (from-to)4702-4710
Number of pages9
JournalJournal of Biological Chemistry
Volume282
Issue number7
DOIs
StatePublished - Feb 16 2007

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Ding, W. X., Ni, H. M., Gao, W., Hou, Y. F., Melan, M. A., Chen, X., Stolz, D. B., Shao, Z. M., & Yin, X. M. (2007). Differential effects of endoplasmic reticulum stress-induced autophagy on cell survival. Journal of Biological Chemistry, 282(7), 4702-4710. https://doi.org/10.1074/jbc.M609267200