The involvement of oxidative stress in tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in HeLa cells
- Authors
- Lee, Myoung Woo; Park, Soon Cheol; Kim, Joung-Hun; Kim, In-Ki; Han, Kun Soo; Kim, Kyung Yong; Lee, Won Bok; Jung, Yong-Keun; Kim, Sung Su
- Issue Date
- Aug-2002
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Apoptosis; Caspase; Reactive oxygen species; Tumor necrosis factor-related apoptosis-inducing ligand
- Citation
- CANCER LETTERS, v.182, no.1, pp 75 - 82
- Pages
- 8
- Journal Title
- CANCER LETTERS
- Volume
- 182
- Number
- 1
- Start Page
- 75
- End Page
- 82
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/57464
- DOI
- 10.1016/S0304-3835(02)00074-5
- ISSN
- 0304-3835
1872-7980
- Abstract
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) serves as an extracellular signal triggering apoptosis in tumor cells. However, the molecular mechanisms leading to the apoptosis are largely unknown. To characterize the molecular events involved in TRAIL-induced apoptosis, we examined the association of reactive oxygen species (ROS) in human adenocarcinoma HeLa cells. In this study, we show strong ROS accumulation upon TRAIL induction, with activation of caspases, followed by apoptosis. The pre-treatment with gamma-glutamylcysteinylglycine or estrogen, both effective antioxidants, significantly attenuated TRAIL-induced apoptosis through the reduction of ROS accumulation and diminished caspases activity. Furthermore, zVAD-fmk, an inhibitor of pan-caspase, effectively inhibited the activation of caspases and prevented apoptosis by TRAIL, although TRAIL-induced ROS generation was not attenuated. These data indicate that ROS may play a role as an upstream mediator of caspases. Taken together, our results suggest that oxidative stress mediates TRAIL-induced apoptosis in HeLa cells. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
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Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
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