Title : ET-18-O-CH3-induced apoptosis is causally linked to COX-2 upregulation in H-ras transformed human breast epithelial cells.

Pub. Date : 2005 Nov 7

PMID : 16253239






4 Functional Relationships(s)
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1 ET-18-O-CH3-induced apoptosis is causally linked to COX-2 upregulation in H-ras transformed human breast epithelial cells. edelfosine prostaglandin-endoperoxide synthase 2 Homo sapiens
2 Contrary to this notion, we have found that a novel alkylphospholipid type antitumor agent ET-18-O-CH3 (1-O-octadecyl-2-O-methyl-glycero-3-phosphocholine) induces COX-2 expression in H-ras transformed human breast epithelial cells (MCF10A-ras) while it causes apoptosis at the same concentration range. edelfosine prostaglandin-endoperoxide synthase 2 Homo sapiens
3 ET-18-O-CH3 enhanced the transcriptional activities of cyclic AMP response element which is a key regulator of COX-2 expression. edelfosine prostaglandin-endoperoxide synthase 2 Homo sapiens
4 Based on these findings, it is likely that ET-18-O-CH3 induces COX-2 expression and production of 15d-PGJ2 which may mediate the ET-18-O-CH3-induced apoptosis in MCF10A-ras cells. edelfosine prostaglandin-endoperoxide synthase 2 Homo sapiens