About this Journal Submit a Manuscript Table of Contents
Gastroenterology Research and Practice
Volume 2012 (2012), Article ID 897678, 9 pages
Research Article

Nutrient Availability Alters the Effect of Autophagy on Sulindac Sulfide-Induced Colon Cancer Cell Apoptosis

1Research Division, Veterans Affairs Medical Center, 5901 E 7th Street, Long Beach, CA 90822, USA
2Department of Medicine, University of California, 101 The City Drive, Irvine, Orange, CA 92868, USA
3UCI Pathology Department, Chao Family Comprehensive Cancer Center, University of California, Irvine 92697, USA
4Neuro-Oncology Program, Chao Comprehensive Cancer Center, UC Irvine School of Medicine, University of California, Irvine, Orange, CA 92868, USA

Received 17 May 2012; Accepted 13 November 2012

Academic Editor: Akira Andoh

Copyright © 2012 Shiun-Kwei Chiou et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Autophagy is a catabolic process by which a cell degrades its intracellular materials to replenish itself. Induction of autophagy under various cellular stress stimuli can lead to either cell survival or cell death via apoptotic and/or autophagic (nonapoptotic) pathways. The NSAID sulindac sulfide induces apoptosis in colon cancer cells. Here, we show that inhibition of autophagy under serum-deprived conditions resulted in significant reductions of sulindac sulfide-induced apoptosis in HT-29 colon cancer cells. In contrast, inhibition of autophagy under conditions where serum is available significantly increased sulindac sulfide-induced apoptosis in HT-29 cells. We previously showed that the apoptosis inhibitor, survivin, plays a role in regulating NSAID-induced apoptosis and autophagic cell death. Here, we show that survivin protein half-life is increased in the presence of autophagy inhibitors under serum-deprived conditions, but not under conditions when serum is available. Thus, the increased levels of survivin may be a factor contributing to inhibition of sulindac sulfide-induced apoptosis under serum-deprived conditions. These results suggest that whether a cell lives or dies due to autophagy induction depends on the balance of factors that regulate both autophagic and apoptotic processes.