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Oncol Lett. 2017 Oct;14(4):5027-5033. doi: 10.3892/ol.2017.6742. Epub 2017 Aug 10.

Ginkgetin induces cell death in breast cancer cells via downregulation of the estrogen receptor.

Author information

1
Division of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, Nowon, Seoul, Gyeonggi 01812, Republic of Korea.
2
School of Life Science and Biotechnology, Korea University, Seongbuk, Seoul, Gyeonggi 02841, Republic of Korea.
3
KIRAMS Radiation Biobank, Korea Institute of Radiological and Medical Sciences, Nowon, Seoul, Gyeonggi 01812, Republic of Korea.
4
Department of Surgery, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Nowon, Seoul, Gyeonggi 01812, Republic of Korea.
5
Laboratory of Chemical Biology and Genomics, Korea Research Institute of Bioscience and Biotechnology, Yuseong, Daejeon, Chungcheong 34141, Republic of Korea.
6
Department of Microbiological Engineering, Kon-Kuk University, Gwangjin, Seoul, Gyeonggi 05029, Republic of Korea.

Abstract

Ginkgetin is a natural biflavonoid isolated from the leaves of Ginkgo biloba, and is characterized by its anti-inflammatory and anti-viral activities. Although numerous studies state that it has also antitumor activity, the anti-proliferative effect of ginkgetin and the underlying mechanism in breast cancer cells have not yet been investigated. In the present study, ginkgetin inhibited the cell viability of MCF-7 and T-47D cells dose-dependently, and suppressed the expression of the estrogen receptor (ER) at the mRNA and protein levels. Among the targets of the ER, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), cyclin D1 and survivin were also downregulated by ginkgetin treatment. The anti-proliferative effects of ginkgetin were sufficient to suppress the growth by estradiol stimulation. However, ginkgetin did not significantly affect the viability of MDA-MB-231 cells, which are ER-negative cells. Furthermore, the knockdown of the ER and an inhibitor of PFKFB3 significantly sensitized MCF-7 and T-47D cells to ginkgetin. These findings suggest that ginkgetin induces cell death in ER-positive breast cancer cells via the inhibition of ER expression and that it is a promising agent for breast cancer treatment.

KEYWORDS:

apoptosis; breast cancer; estrogen receptor; ginkgetin

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