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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2004.1
- 수록면
- 444 - 453 (10page)
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초록· 키워드
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Δ12-Prostaglandin (PG) J2 is known to elicit an
anti-neoplastic effects via apoptosis induction.
Previous study showed Δ12-PGJ2-induced apoptosis
utilized caspase cascade through cytochrome
c-dependent pathways in HeLa cells. In
this study, the cellular mechanism of Δ12-PGJ2-
induced apoptosis in HeLa cells, specifically,
the role of two m itochondrial factors; bcl-2 and
apoptosis-inducing factor (AIF) was investigated.
Bcl-2 attenuated Δ12-PGJ2-induced caspase
activation, loss of mitochondrial transmembrane
potential (Δψm), nuclear fragmentation,
DNA laddering, and growth curve inhibition for
approximately 24 h, but not for longer time. AIF
was not released from mitochondria, even if the
Δψm was dissipated. One of the earliest events
observed in Δ12-PGJ2-induced apoptotic events
was dissipation of Δψm, the process known to
be inhibited by bcl-2. Pre-treatment of z-VADfmk,
the pan-caspase inhibitor, resulted in the
attenuation of Δψm depolarization in Δ12-PGJ2-
induced apoptosis. Up-regulation of Sox-4 protein
by Δ12-PGJ2 was observed in HeLa and
bcl-2 overexpressing HeLa B4 cell lines. Bcl-2
overexpression did not attenuate the expression
of Sox-4 and its expression coincided with other
apoptotic events. These results suggest tha t
Δ12-PGJ2 induced Sox-4 expression may activate
another upstream caspases excluding the
caspase 9-caspase 3 cascade of mitochondrial
pathway. These and previous findings together
suggest that Δ12-PGJ2-induced apoptosis in HeLa
cells is caspase-dependent, AIF-independent
events which may be affected by Sox-4 protein
expression up-regulated by Δ12-PGJ2.
목차
등록된 정보가 없습니다.
참고문헌 (30)
참고문헌 신청
/ / Activation of heat shocktranscription factors by Δ12-prostaglandin J2 and its inhibitionby intracellular glutathione : 2457 ~ 64
/ / Mode of action in G1 arrest andpreclinical results : 161 ~ 5
/ / ProstaglandinA2 and Δ12-prostaglandin J2 induce apoptosis in L1210 cells : 209 ~ 14
/ 1996 / Regulation of BiP gene expression by cyclopentenoneprostaglandins through unfolded protein responseelement kita (y) : 16609 ~ 13
/ 1998 / Mitochondrial cytochromec release in apoptosis occurs upstream of DEVD-specificcaspase activation and independently of mitochondrial transmembranedepolarization : 37
/ / Mode of action in G1 arrest andpreclinical results : 161 ~ 5
/ / ProstaglandinA2 and Δ12-prostaglandin J2 induce apoptosis in L1210 cells : 209 ~ 14
/ 1996 / Regulation of BiP gene expression by cyclopentenoneprostaglandins through unfolded protein responseelement kita (y) : 16609 ~ 13
/ 1998 / Mitochondrial cytochromec release in apoptosis occurs upstream of DEVD-specificcaspase activation and independently of mitochondrial transmembranedepolarization : 37
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