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.