ABSTRACT Background: EGCG is the most active principle present in green tea, demonstrated to have chemopreventive action and to kill cancer cells selectively. As a previous study found that catechins could compete with 17-alpha-estradiol for binding to estrogen receptors alpha (ER), we asked whether EGCG could regulate ER action. Methods: We used MCF-7, a breast carcinoma cell line having great ER expression. The cells were treated with various EGCG concentrations and cell viability evaluated by MTT assay. ER and pS2 expression were analyzed by RT-PCR after RNA extraction. To better define EGCG action in relation to ER, we studied EGCG cytotoxicity on MCF-7 resistant to tamoxifen (MCF-7tam), MCF-7 treated with 10-7 M ICI 780,181 for 8 days, and MDA-MB-231, a cell line that lacked ER, by Flow Cytometry (FCM). Results: Both ER and pS2 mRNA were expressed in samples treated with low EGCG concentration (30 µg/ml). At this concentration, no cell change was detectable. In contrast, pS2 expression was lost in samples treated with 100 µg/ml EGCG for 24 hours, indicating ER functional inactivation. EGCG cytotoxicity was lower when ER was not present (MDA-MB-231) or inactivated (by tamoxifen or ICI 780,181). Conclusions: Functionally active ER may have a role in EGCG cytotoxicity, increasing the sensitivity to the drug. As greater EGCG concentrations could also kill cells resistant to tamoxifen or treated by 10-7 M ICI 780,181, EGCG ought to be better investigated in breast carcinoma cells treated with drugs targeted to steroid receptors as a potential complement of therapy.
F. Farabegoli, C. Barbi, E. Lambertini, R. Piva (2007). (-)-Epigallocatechin-3-gallate down regulates estrogen receptor alpha function in MCF-7 breast carcinoma cells. CANCER DETECTION AND PREVENTION, 31(6), 499-504 [10.1016/j.cdp.2007.10.018].
(-)-Epigallocatechin-3-gallate down regulates estrogen receptor alpha function in MCF-7 breast carcinoma cells
FARABEGOLI, FULVIA;BARBI, CRISTIANA;
2007
Abstract
ABSTRACT Background: EGCG is the most active principle present in green tea, demonstrated to have chemopreventive action and to kill cancer cells selectively. As a previous study found that catechins could compete with 17-alpha-estradiol for binding to estrogen receptors alpha (ER), we asked whether EGCG could regulate ER action. Methods: We used MCF-7, a breast carcinoma cell line having great ER expression. The cells were treated with various EGCG concentrations and cell viability evaluated by MTT assay. ER and pS2 expression were analyzed by RT-PCR after RNA extraction. To better define EGCG action in relation to ER, we studied EGCG cytotoxicity on MCF-7 resistant to tamoxifen (MCF-7tam), MCF-7 treated with 10-7 M ICI 780,181 for 8 days, and MDA-MB-231, a cell line that lacked ER, by Flow Cytometry (FCM). Results: Both ER and pS2 mRNA were expressed in samples treated with low EGCG concentration (30 µg/ml). At this concentration, no cell change was detectable. In contrast, pS2 expression was lost in samples treated with 100 µg/ml EGCG for 24 hours, indicating ER functional inactivation. EGCG cytotoxicity was lower when ER was not present (MDA-MB-231) or inactivated (by tamoxifen or ICI 780,181). Conclusions: Functionally active ER may have a role in EGCG cytotoxicity, increasing the sensitivity to the drug. As greater EGCG concentrations could also kill cells resistant to tamoxifen or treated by 10-7 M ICI 780,181, EGCG ought to be better investigated in breast carcinoma cells treated with drugs targeted to steroid receptors as a potential complement of therapy.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
