Abstract
The effect of celecoxib, a cyclooxygenase-2 selective inhibitor, on a human cervical cancer cell line, HeLa cells, was examined. We found that celecoxib increased DNA ladder formation and the activity of caspase-3, indicating that celecoxib induced apoptosis in HeLa cells. Celecoxib suppressed the expression of an anti-apoptotic protein, survivin, in both protein and mRNA levels. The overexpression of survivin overrode caspase-3 activation induced by celecoxib. Subsequently, we performed luciferase reporter assay with the reporter vector containing human survivin promoter region and electrophoretic mobility shift assay and found that the -75 to -66 bp region relative to the initiating codon played an important role in celecoxib action to suppress survivin promoter activity. Our findings might provide a new insight into the anti-cancer effects of celecoxib.
| Original language | English |
|---|---|
| Pages (from-to) | 1166-1171 |
| Number of pages | 6 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 357 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Jun 15 2007 |
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All Science Journal Classification (ASJC) codes
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology
Cite this
Celecoxib induces apoptosis by inhibiting the expression of survivin in HeLa cells. / Fukada, Kazuhiro; Takahashi-Yanaga, Fumi; Sakoguchi-Okada, Naoko; Shiraishi, Fumie; Miwa, Yoshikazu; Morimoto, Sachio; Sasaguri, Toshiyuki.
In: Biochemical and Biophysical Research Communications, Vol. 357, No. 4, 15.06.2007, p. 1166-1171.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Celecoxib induces apoptosis by inhibiting the expression of survivin in HeLa cells
AU - Fukada, Kazuhiro
AU - Takahashi-Yanaga, Fumi
AU - Sakoguchi-Okada, Naoko
AU - Shiraishi, Fumie
AU - Miwa, Yoshikazu
AU - Morimoto, Sachio
AU - Sasaguri, Toshiyuki
PY - 2007/6/15
Y1 - 2007/6/15
N2 - The effect of celecoxib, a cyclooxygenase-2 selective inhibitor, on a human cervical cancer cell line, HeLa cells, was examined. We found that celecoxib increased DNA ladder formation and the activity of caspase-3, indicating that celecoxib induced apoptosis in HeLa cells. Celecoxib suppressed the expression of an anti-apoptotic protein, survivin, in both protein and mRNA levels. The overexpression of survivin overrode caspase-3 activation induced by celecoxib. Subsequently, we performed luciferase reporter assay with the reporter vector containing human survivin promoter region and electrophoretic mobility shift assay and found that the -75 to -66 bp region relative to the initiating codon played an important role in celecoxib action to suppress survivin promoter activity. Our findings might provide a new insight into the anti-cancer effects of celecoxib.
AB - The effect of celecoxib, a cyclooxygenase-2 selective inhibitor, on a human cervical cancer cell line, HeLa cells, was examined. We found that celecoxib increased DNA ladder formation and the activity of caspase-3, indicating that celecoxib induced apoptosis in HeLa cells. Celecoxib suppressed the expression of an anti-apoptotic protein, survivin, in both protein and mRNA levels. The overexpression of survivin overrode caspase-3 activation induced by celecoxib. Subsequently, we performed luciferase reporter assay with the reporter vector containing human survivin promoter region and electrophoretic mobility shift assay and found that the -75 to -66 bp region relative to the initiating codon played an important role in celecoxib action to suppress survivin promoter activity. Our findings might provide a new insight into the anti-cancer effects of celecoxib.
UR - http://www.scopus.com/inward/record.url?scp=34247886162&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=34247886162&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2007.04.077
DO - 10.1016/j.bbrc.2007.04.077
M3 - Article
C2 - 17466271
AN - SCOPUS:34247886162
VL - 357
SP - 1166
EP - 1171
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 4
ER -