Naringenin: a partial agonist on estrogen receptor in T47D-KBluc breast cancer cells.

Naringenin is present abundantly in citrus fruits and is one of the natural alternatives to synthetic estrogen, but the mechanism of how naringenin functions is not well known. Our study revealed that the relative estrogenic potency of the substances was E2 > genistein > naringenin. Naringenin (at 5 μM) was found to repress both luciferase activity and pS2 mRNA expression, which was induced by E2 (at 0.1 μM) or genistein (at 5 μM). Naringenin, as well as E2 and genistein, was found to modulate the transcription of pS2 and TGFβ3 in T47D-KBluc cells through an estrogen receptor-dependent mechanism. Results of our study indicated that naringenin was a weak estrogen agonist that exhibits anti-estrogenic effect in estrogen-rich states and estrogenic activity in estrogen-deficient states in T47D-KBluc breast cancer cells.