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Carcinogenesis Advance Access originally published online on April 5, 2006
Carcinogenesis 2006 27(10):1961-1969; doi:10.1093/carcin/bgl027
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

GADD153 mediates celecoxib-induced apoptosis in cervical cancer cells

Su-Hyeong Kim1, Chang-Il Hwang2, Woong-Yang Park2, Je-Ho Lee4 and Yong-Sang Song1,3,*

1 Cancer Research Institute, Seoul National University College of Medicine 28 Yungun-Dong, Chongno-Ku, Seoul 110-744, Korea
2 Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine 28 Yungun-Dong, Chongno-Ku, Seoul 110-744, Korea
3 Department of Obstetrics and Gynecology, Seoul National University College of Medicine 28 Yungun-Dong, Chongno-Ku, Seoul 110-744, Korea
4 Molecular Therapy Research Center, Samsung Medical Center, School of Medicine Sungkyunkwan University 50 Ilwon-dong, Kangnam-ku, Seoul 135-710, Korea

*To whom correspondence should be addressed. Tel: +82 2 2072 2822; Fax: +82 2 3668 7401; E-mail: yssong{at}snu.ac.kr

Celecoxib, a selective cyclooxygenase-2 inhibitor, is known to possess anti-inflammatory activity and also induces apoptosis in various types of cancer cells. Here, we examined the molecular mechanism of celecoxib-induced apoptosis in cervical cancer cell lines (HeLa, CaSki and C33A). Screening of a cDNA microarray chip containing 225 different genes revealed that GADD153 (growth arrest and DNA damage inducible gene), a transcription factor involved in apoptosis, showed the strongest differential expression following celecoxib treatment in all three cervical cancer cell lines. Notably, siRNA-induced silencing of GADD153 suppressed celecoxib-induced apoptosis in all three cell lines, and exogenous expression of GADD153 triggered apoptosis in cervical cancer cells in the absence of other apoptotic stimuli. A luciferase reporter gene assay and mRNA stability tests revealed that the expression of GADD153 was regulated at both the transcriptional and post-transcriptional levels following celecoxib treatment. The region between –649 and –249, containing an intact C/EBP-ATF binding site, is required for celecoxib-induced stimulation of GADD153 promoter activity. In terms of signaling pathway, addition of the NF-{kappa}B inhibitor, N-tosyl-L-phenylalanyl-chloromethyl ketone, had no effect on GADD153 expression levels. Celecoxib treatment induced Bak expression, whereas cell transfected with siGADD153 showed lower levels of celecoxib-induced Bak upregulation. These novel findings collectively suggest that GADD153 may play a key role in celecoxib-induced apoptosis in cervical cancer cells by regulating the expression of proapoptotic proteins such as Bak.


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