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Titolo:
Geranylgeraniol, an intermediate product in mevalonate pathway, induces apoptotic cell death in human hepatoma cells: Death receptor-independent activation of caspase-8 with down-regulation of Bcl-xL expression
Autore:
Takeda, Y; Nakao, K; Nakata, K; Kawakami, A; Ida, H; Ichikawa, T; Shigeno, M; Kajiya, Y; Hamasaki, K; Kato, Y; Eguchi, K;
Indirizzi:
Nagasaki Univ, Sch Med, Dept Internal Med 1, Nagasaki 8528501, Japan Nagasaki Univ Nagasaki Japan 8528501 rnal Med 1, Nagasaki 8528501, Japan Nagasaki Univ, Hlth Res Ctr, Nagasaki 8528501, Japan Nagasaki Univ Nagasaki Japan 8528501 th Res Ctr, Nagasaki 8528501, Japan
Titolo Testata:
JAPANESE JOURNAL OF CANCER RESEARCH
fascicolo: 9, volume: 92, anno: 2001,
pagine: 918 - 925
SICI:
0910-5050(200109)92:9<918:GAIPIM>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
2ND PRIMARY TUMORS; HEPATOCELLULAR-CARCINOMA; ALPHA-FETOPROTEIN; HL-60 CELLS; KAPPA-B; PROTEIN; ACID; CHEMOPREVENTION; RECURRENCE; INHIBITION;
Keywords:
geranylgeraniol; apoptosis; caspase-8; Bcl-xL; hepatocellular carcinoma;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Eguchi, K Nagasaki Univ, Sch Med, Dept Internal Med 1, 1-7-1 Sakamoto, Nagasaki 8528501, Japan Nagasaki Univ 1-7-1 Sakamoto Nagasaki Japan 8528501 8501, Japan
Citazione:
Y. Takeda et al., "Geranylgeraniol, an intermediate product in mevalonate pathway, induces apoptotic cell death in human hepatoma cells: Death receptor-independent activation of caspase-8 with down-regulation of Bcl-xL expression", JPN J CANC, 92(9), 2001, pp. 918-925

Abstract

Geranylgeraniol (GGOH), an intermediate of mevalonate metabolism, is knownto induce apoptosis in various lines of cancer cells. The present study was undertaken to clarify the signaling pathways of apoptosis induced by GGOHin human hepatoma cells. HuH-7 human hepatoma cells were incubated in the absence or presence of GGOH. Activation of caspase-8/-9/-3 in HuH-7 cells was found after 8 h treatment with GGOH, at which time DNA fragmentation andloss of mitochondrial transmembrane potential (Delta Psim) occurred. HuH-7cells do not express Bcl-2; however, downregulation of Bcl-xL expression preceded activation of the caspase cascade in GGOH-treated HuH-7 cells, while Bax expression was not changed by GGOH treatment. Addition of caspase inhibitors restored the decreased cell viability of HuH-7 cells by GGOH, including Delta Psim, to the baseline level, which indicated that caspase triggers mitochondria-dependent apoptotic pathways in GGOH-treated HuH-7 cells. Similarly, GGOH-mediated apoptosis of HuH-7 cells was clearly prevented by coadministration of ursodeoxycholic acid (UDCA), which led to restoration ofthe level of Bcl-xL expression. Activation of caspase-8/-9/-3, as well as Delta Psim, by GGOH treatment was suppressed by addition of UDCA. Our results indicate that activation of the caspase cascade initiating from caspase-8, which could be accelerated by down-regulation of Bcl-xL expression, plays a key role in an apoptotic process induced by GGOH in human hepatoma cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 22:32:39