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Titolo:
Potential role of caspase-3 and-9 in arsenic trioxide-mediated apoptosis in PCI-1 head and neck cancer cells
Autore:
Seol, JG; Park, WH; Kim, ES; Jung, CW; Hyun, JM; Lee, YY; Kim, BK;
Indirizzi:
Seoul Natl Univ, Coll Med, Dept Internal Med, Canc Res Ctr, Seoul 110744, South Korea Seoul Natl Univ Seoul South Korea 110744 Ctr, Seoul 110744, South Korea Chung Ang Univ, Coll Med, Dept Internal Med, Seoul 140757, South Korea Chung Ang Univ Seoul South Korea 140757 l Med, Seoul 140757, South Korea Han Yang Univ Hosp, Dept Internal Med, Seoul 133792, South Korea Han Yang Univ Hosp Seoul South Korea 133792 d, Seoul 133792, South Korea
Titolo Testata:
INTERNATIONAL JOURNAL OF ONCOLOGY
fascicolo: 2, volume: 18, anno: 2001,
pagine: 249 - 255
SICI:
1019-6439(200102)18:2<249:PROCAI>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE PROMYELOCYTIC LEUKEMIA; CYTOCHROME-C; MOLECULAR MECHANISMS; ICE/CED-3 PROTEASE; DOWN-REGULATION; RETINOIC ACID; IN-VITRO; ACTIVATION; BCL-2; DEATH;
Keywords:
As2O3; caspase-3; caspase-9; apoptosis; PCI-1 cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Kim, BK Seoul Natl Univ Hosp, Dept Internal Med, Div Hematol Oncol, 28 Yongon Dong, Seoul 110744, South Korea Seoul Natl Univ Hosp 28 Yongon Dong Seoul South Korea 110744 orea
Citazione:
J.G. Seol et al., "Potential role of caspase-3 and-9 in arsenic trioxide-mediated apoptosis in PCI-1 head and neck cancer cells", INT J ONCOL, 18(2), 2001, pp. 249-255

Abstract

Arsenic trioxide (As2O3) has been shown to inhibit the proliferation of hematologic malignant cells. Previously, we reported that As2O3 had an antitumoral effect in head and neck cancer. Here, we investigated the induction of apoptosis and its mechanism in PCI-1 head and neck squamous carcinoma cells, after treatment with As2O3. Treatment with 2 muM of As2O3 caused apoptosis in PCI-1 cells following 3 days of exposure, which was detected by the annexin V-PI and DAPI staining methods. The cell death population was markedly increased, being 88% larger than the As2O3- untreated control cells. Toaddress the mechanism of apoptosis, a Western blot assay was performed, showing that Bax was up-regulated without a change in Bcl-2. Activation of caspase-9 during As2O3-induced apoptosis was substantiated by monitoring the proteolysis of the caspase-9, which was associated with an increase of Apaf-1 and cytochrome c protein. PCI-1 cells rapidly changed the mitochondria membrane potential (Delta psi (m)) after addition of As2O3. Furthermore, activation of caspase-3 was demonstrated by monitoring the proteolysis of the caspase-3 and by measuring caspase-3 activity with a fluorogenic substrate,which was associated with the cleavage of poly(ADP-ribose) polymerase. To examine the in vivo effect of As2O3, C3H mouse inoculated with syngenic SCC7 cells was treated by intratumoral injection of As2O3 (300 mug) every day,demonstrating that tumor mass was dramatically reduced on day 4, and revealed induction of apoptosis by TUNEL assay. These results suggest that apoptosis of PCI-1 cells by As2O3 is induced by activation of caspase-3 via cytochrome c, caspase-9 and Apaf-1 complex.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 14:37:36