15-Lipoxygenase-1 mediates nonsteroidal anti-inflammatory drug-induced apoptosis independently of cyclooxygenase-2 in colon cancer cells.
Cancer Res
; 60(24): 6846-50, 2000 Dec 15.
Article
em En
| MEDLINE
| ID: mdl-11156377
ABSTRACT
We previously found (I. Shureiqi et al., Carcinogenesis (Lond.), 20 1985-1995, 1999; I. Shureiqi et al, J. Natl. Cancer Inst., 92 1136-1142, 2000) that (a) 15-lipoxygenase-1 (15-LOX-1) protein and its product 13-S-hydroxyoctadecadienoic acid (13-S-HODE) are decreased; and (b) nonsteroidal anti-inflammatory drug (NSAID)-induced 15-LOX-1 expression is critical to NSAID-induced apoptosis in colorectal cancer cells expressing cyclooxygenase-2 (COX-2). We used the NSAIDs sulindac sulfone (COX-2-independent) and NS-398 (a COX-2 inhibitor) to assess NSAID upregulation of 15-LOX-1 in relation to COX-2 inhibition during NSAID-induced apoptosis in the DLD-1 (COX-2-negative) colon cancer cell line. We found that (a) NSAIDs up-regulated 15-LOX-1, which preceded apoptosis; and (b) 15-LOX-1 inhibition blocked NSAID-induced apoptosis, which was restored by 13-S-HODE but not by its parent, linoleic acid. NSAIDs can induce apoptosis in colon cancer cells via up-regulation of 15-LOX-1 in the absence of COX-2.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Araquidonato 15-Lipoxigenase
/
Anti-Inflamatórios não Esteroides
/
Prostaglandina-Endoperóxido Sintases
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Apoptose
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Neoplasias do Colo
/
Isoenzimas
Limite:
Humans
Idioma:
En
Revista:
Cancer Res
Ano de publicação:
2000
Tipo de documento:
Article
País de afiliação:
Estados Unidos