TY - JOUR
T1 - Antitumor effect of green tea polyphenol epigallocatechin-3-gallate in ovarian carcinoma cells
T2 - Evidence for the endothelin-1 as a potential target
AU - Spinella, Francesca
AU - Rosanò, Laura
AU - Decandia, Samantha
AU - Di Castro, Valeriana
AU - Albini, Adriana
AU - Elia, Giacomo
AU - Natali, Pier Giorgio
AU - Bagnato, Anna
PY - 2006/6
Y1 - 2006/6
N2 - 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 ET AR by ET-1 plays a critical role in tumor growth and progression.
AB - 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 ET AR by ET-1 plays a critical role in tumor growth and progression.
KW - EGCG
KW - Endothelin-1
KW - ET receptor
KW - Green tea
KW - Ovarian carcinoma
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M3 - Article
C2 - 16741061
AN - SCOPUS:33744902332
VL - 231
SP - 1123
EP - 1127
JO - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)
JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)
SN - 0037-9727
IS - 6
ER -