 | |  | |  | |  | |  | |  | |  | |  |
| IJCEM Copyright © 2008-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711 |
Int J Clin Exp Med 2013;6(10):890-899
Original Article
Naringenin: a partial agonist on estrogen receptor in T47D-KBluc breast cancer cells
Sunzoo Kim, Tae In Park
Department of Pathology, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu, South
Korea
Received October 8, 2013; Accepted October 20, 2013; Epub October 25, 2013; Published October 30, 2013
Abstract: 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. (IJCEM1310008).
Keywords: pS2, TGFβ3, genistein, selective estrogen receptor modulator
Address correspondence to: Dr. Tae In Park, Department of Pathology, Kyungpook National University Hospital, Kyungpook National
University School of Medicine, 50 Samduk-dong 2 Ga, Jung-gu, Daegu, South Korea Zip code: 700-721. Tel: +82-53-420-5247; Fax:
+82-53-426-1525; E-mail: tipark@knu.ac.kr
Original Article
Naringenin: a partial agonist on estrogen receptor in T47D-KBluc breast cancer cells
Sunzoo Kim, Tae In Park
Department of Pathology, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu, South
Korea
Received October 8, 2013; Accepted October 20, 2013; Epub October 25, 2013; Published October 30, 2013
Abstract: 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. (IJCEM1310008).
Keywords: pS2, TGFβ3, genistein, selective estrogen receptor modulator
Address correspondence to: Dr. Tae In Park, Department of Pathology, Kyungpook National University Hospital, Kyungpook National
University School of Medicine, 50 Samduk-dong 2 Ga, Jung-gu, Daegu, South Korea Zip code: 700-721. Tel: +82-53-420-5247; Fax:
+82-53-426-1525; E-mail: tipark@knu.ac.kr
