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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.1
- 수록면
- 293 - 300 (8page)
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초록· 키워드
오류제보하기
Cyclopentenone prostaglandins (PGs) have antiproliferative
activity on various tumor cell growth
in vitro. Particularly, 9-deoxy-∆9,12-13,14-dihydro
PGD2 (∆12-PGJ2) was reported for its antineoplastic
and apoptotic effects on various cancer cells,
but its mechanism inducing apoptosis is still not
clear. In this study, we have characterized apoptosis
induced by ∆12-PGJ2 in HeLa cells. Treatment
of ∆12-PGJ2 induced apoptosis as indicated
by DNA fragmentation, chromatin condensation,
and formation of apoptotic body. We also observed
release of cytochrome c from mitochondria
and activation of caspase cascade including
caspase-3, -8, and -9. And the pan-caspase
inhibitor z-Val-Ala-Asp (OMe) fluoromethyl-ketone
(z-VAD-fmk) and Q-Val-Asp (OMe)-CH2-OPH (Q-VD
(OMe)-OPH) prevented cell death induced by ∆12-
PGJ2 showing participation of caspases in this
process. However, protein expression level of
Bcl-2 family was not altered by ∆12-PGJ2, seem s
to have no effect on HeLa cell apoptosis. And
ZB4, an antagonistic Fas-antibody, exerted no
effect on the activation of caspase 8 indicating
that Fas receptor-ligand interaction was not
involved in this pathway. Treatment of ∆12-PGJ2
also leads to suppression of nuclear factor κB
(NF-κB) as indicated by nuclear translocation of
p65/RelA and c-Rel and its DNA binding ability
analyzed by EMSA. Taken together, our results
suggest that ∆12-PGJ2-induced apoptosis in HeLa
cell utilized caspase cascade without Fas receptor-
ligand interaction and accompanied with
NF-κB inactivation.
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