Antitumor effect of green tea polyphenol epigallocatechin-3-gallate in ovarian carcinoma cells: evidence for the endothelin-1 as a potential target

F Spinella, L Rosanò, S Decandia… - Experimental …, 2006 - journals.sagepub.com
F Spinella, L Rosanò, S Decandia, V Di Castro, A Albini, G Elia, PG Natali, A Bagnato
Experimental Biology and Medicine, 2006journals.sagepub.com
The green tea polyphenol, epigallocatechin-3-gallate (EGCG), has been shown to prevent
cancer; however, a precise mechanism responsible for tumor growth inhibition has not yet
been clearly described. The endothelin (ET) A receptor (ETAR)/ET-1 autocrine pathway is
overexpressed in ovarian carcinoma and triggers tumor growth, neoangiogenesis, and
invasion. These latter tumor-promoting effects are mediated through the activation of
cyclooxygenase (COX)-1–and COX-2–dependent pathways by ET-1. In the present study …
The green tea polyphenol, epigallocatechin-3-gallate (EGCG), has been shown to prevent cancer; however, a precise mechanism responsible for tumor growth inhibition has not yet been clearly described. The endothelin (ET) A receptor (ETAR)/ET-1 autocrine pathway is overexpressed in ovarian carcinoma and triggers tumor growth, neoangiogenesis, and invasion. These latter tumor-promoting effects are mediated through the activation of cyclooxygenase (COX)-1– and COX-2–dependent pathways by ET-1. In the present study, pretreatment of HEY and OVCA 433 ovarian carcinoma cell lines with green tea and EGCG inhibited ET-1/ETAR expression, ETAR-mediated COX-1/2 mRNA expression, and COX-2 promoter activity. These effects were associated with a significant reduction in the COX-1/2–derived prostaglandin E2 (PGE2) production. These results provide a novel insight into the mechanism by which EGCG, by affecting ETAR-dependent COX-1/2 pathways may inhibit ovarian tumors suggesting that EGCG may be useful in preventing and treating ovarian carcinoma in which activation of ETAR by ET-1 plays a critical role in tumor growth and progression.
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