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Protective role of cytosolic 2-cys peroxiredoxin in the TNF-α-induced apoptotic death of human cancer cells

Title
Protective role of cytosolic 2-cys peroxiredoxin in the TNF-α-induced apoptotic death of human cancer cells
Authors
Lee J.Y.Jung H.J.Song I.S.Williams M.S.Choi C.Rhee S.G.Kim J.Kang S.W.
Ewha Authors
이서구강상원
SCOPUS Author ID
이서구scopusscopus; 강상원scopus
Issue Date
2009
Journal Title
Free Radical Biology and Medicine
ISSN
0891-5849JCR Link
Citation
vol. 47, no. 8, pp. 1162 - 1171
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Cytosolic 2-cys peroxiredoxin (2-cysPrx) exhibiting thioredoxin-dependent hydroperoxide reductase activity has been demonstrated to be involved in a number of signaling processes, such as receptor tyrosine kinase and MAP kinase activation. However, its role in the cell death pathway has yet to be elucidated. Here we show that cytosolic 2-cysPrx suppresses the TNF-α-induced apoptosis of human cervical cancer cells in a caspase-8-dependent manner. The HeLa cervical cancer cells expressing a dominant negative mutant (DN) of a cytosolic 2-cysPrx manifested remarkable increase in intracellular reactive oxygen species level, which was counteracted by catalase administration, and apoptotic cell death induced by combined treatment of TNF-α and cycloheximide compared to the control (CT) cells. Similarly, the DN cells were also susceptible to apoptosis induced by the TNF-related apoptosis-inducing ligand. The apoptosis enhanced by DN expression was shown to be dependent on a typical FADD/caspase pathway. The DN cells undergoing apoptosis showed enhanced caspase-8 and -3 activations, as compared to the CT cells. In contrast, there was no difference observed in the sustained JNK activation between CT and DN cells. Thus, this study illustrates that intracellular reactive oxygen species regulated by cytosolic 2-cysPrx is involved in the TNF-α-induced apoptotic cell death via controlling caspase activation. © 2009 Elsevier Inc. All rights reserved.
DOI
10.1016/j.freeradbiomed.2009.07.027
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일반대학원 > 생명·약학부 > Journal papers
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