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The anticancer activity of genistein is increased in estrogen receptor beta 1-positive breast cancer cells

Authors Jiang H, Fan JJ, Cheng L, Hu P, Liu RB

Received 1 August 2018

Accepted for publication 3 October 2018

Published 14 November 2018 Volume 2018:11 Pages 8153—8163


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Leo Jen-Liang Su

Hua Jiang,1,* Jingjing Fan,2,* Lin Cheng,1 Pan Hu,1 Renbin Liu1

1Department of Breast and Thyroid Surgery, Breast Cancer Center, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, People’s Republic of China; 2Department of Breast and Neck Surgery, Xinjiang Medical University Affiliated Tumor Hospital, Urumqi, Xinjiang 830011, People’s Republic of China

*These authors contributed equally to this work

Background: Most breast cancers are estrogen dependent and were sensitive to endocrine therapy, and genistein (GEN) shows strong affinity with human oestrogen receptor beta (ERβ).
Purpose: The present study aimed to investigate the anticancer activity of GEN in breast cancer cell lines that constitutively expressing ERβ1 in vitro and in vivo.
Methods: MCF-7/ERβ1 and MDA-MB-231/ERβ1 cell sub-lines were established through lentiviral infection. Then, cells were treated with increasing concentrations of GEN (10-6 mol/l, 10-5 mol/l and 10-4 mol/l) for 48 h, and cell proliferation, cell cycle analyses were performed to investigate different biological characteristics of ERβ1-overexpressing cell lines. Studies in vivo were also performed to investigate the effects of dietary GEN on MCF-7/ERβ1 and MDA-MB-231/ERβ1 cells implanted mice.
Results: Results showed that compared to parental cells, GEN inhibited the proliferation ability of MCF-7/ERβ1 cells to a greater extent, especially at high concentrations. MDA-MB-231 cells were also inhibited by high doses of GEN, but the overexpressed ERβ1 did not enhance the anti-proliferative effect on MDA-MB-231 cells. ERβ1 arrested cells in G2/M phase, and GEN arrested cells in G0/G1, which led to a combinatorial effect on cell cycle blockade. Furthermore, ERβ1 increased the anti-tumour activity of dietary GEN in MCF-7/ERβ1 subcutaneous tumour models. Our data indicated that ERβ1 increased the anticancer efficacy of GEN in MCF-7 cells by affecting cell cycle transition.
Conclusion: As a result, GEN could be a potential therapeutic agent for ERβ1-positive cancer.

Keywords: breast cancer, estrogen receptor beta 1, genistein, MCF-7 cells, MDA-MB-231 cells, estrogen receptor alpha

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