Activation of SAPK and increase in Bak levels during ceramide and indomethacin-induced apoptosis in HT29 cells
The Korean Journal of Physiology and Pharmacology
; : 75-82, 1999.
Article
em En
| WPRIM
| ID: wpr-728428
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ABSTRACT
It has been reported that activation of sphingomyelin pathway and nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit the promotion of colon carcinoma. Ceramide, a metabolite of sphingomyelin, and indomethacin were shown to induce apoptosis in colon carcinoma cells. However, the mechanisms of ceramide- and indomethacin-induced apoptosis in the colon carcinoma cells are not clearly elucidated. Recent studys showed that indomethacin-induced apoptosis in colon cancer cells through the cyclooxygenase-independent pathways, and that may be mediated by generation of ceramide. In this study, we compared effects of ceramide and indomethacin on important modulators of apoptotic processes in HT29 cells, a human colon cancer cell line. Ceramide and indomethacin induced apoptosis dose- and time-dependently. Ceramide and indomethacin increased stress-activated protein kinase (SAPK) activity, and decreased mitogen-activated protein kinase (MAPK) activity. The expression of Bak was increased by the treatment of ceramide and indomethacin. The expression of other Bcl-2 related proteins (Mcl-1, Bcl-XL, Bax) which were known to be expressed in colon epithelial cells was not changed during the ceramide- and indomethacin-induced apoptosis. Our results suggest that ceramide and indomethacin share common mechanisms for induction of apoptosis in HT29 cells.
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Índice:
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Assunto principal:
Proteínas Quinases
/
Linhagem Celular
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Indometacina
/
Apoptose
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Colo
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Neoplasias do Colo
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Células HT29
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Células Epiteliais
Limite:
Humans
Idioma:
En
Revista:
The Korean Journal of Physiology and Pharmacology
Ano de publicação:
1999
Tipo de documento:
Article