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Quercetin induces type‐II estrogen‐binding sites in estrogen‐receptor‐negative (MDA‐MB231) and estrogen‐receptor‐positive (MCF‐7) human breast‐cancer cell lines
Author(s) -
Scambia G.,
Mancuso S.,
Panici P. Benedetti,
De Vincenzo R.,
Ferrandina G.,
Bonanno G.,
Ranelletti F. O.,
Piantelli M.,
Capelli A.
Publication year - 1993
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910540318
Subject(s) - estrogen receptor , mcf 7 , estrogen , cycloheximide , receptor , endocrinology , medicine , chemistry , quercetin , estrogen receptor alpha , cell , estrogen receptor beta , biology , cell culture , cancer cell , cancer , biochemistry , breast cancer , human breast , genetics , antioxidant
We show that flavonoids positively regulate type‐II estrogen‐binding site (type‐ll EBS) levels both in MCF‐7 (ER‐positive) and in MDA‐MB231 (ER‐negative) breast‐cancer cells. Type‐ll EBS were measured by a whole‐cell assay at 4°C for 2.5 hr using [ 3 H]‐estradiol as tracer. In both cell lines the effect of quercetin (Q) was dose‐related and already evident after 12 hr of Q treatment. The increase of type‐ll EBS levels after Q exposure requires both RNA and protein synthesis, since actinomycin D and cycloheximide completely abolished the stimulatory effect. The ability of flavonoids in inducing type‐ll EBS is well correlated with their relative binding affinity for type‐ll EBS. The flavonoid‐induced enhancement of type‐ll EBS levels is accompanied by increased sensitivity of cancer cells to the inhibitory effect of low Q concentrations. Our data suggest that type‐ll EBS are ligand‐regulated receptors.