NF-κB-dependency and consequent regulation of IL-8 in echinomycin-induced apoptosis of HT-29 colon cancer cells

2008 ◽  
Vol 32 (10) ◽  
pp. 1207-1214 ◽  
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J PARK ◽  
J CHANG ◽  
K BAE ◽  
K LEE ◽  
S CHOI ◽  
...  
2016 ◽  
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Lin Yang ◽  
Yanqing Liu ◽  
Mei Wang ◽  
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Xiaoyun Dong ◽  
...  

2007 ◽  
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Y. K. LEE ◽  
O. J. PARK

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Min Jeong Sin ◽  
...  

2009 ◽  
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Hee-Sun Yang ◽  
Kyoung-Wuk Park ◽  
Jae-Yong Kim ◽  
Mi-Kyung Lee ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-9
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Shiun-Kwei Chiou ◽  
Neil Hoa ◽  
Lisheng Ge ◽  
Martin R. Jadus

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.


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