6,7,4 '-Trihydroxyisoflavone suppressed the estrogen receptor negative breast cancer growth via regulating glycogen synthase kinase-3 beta/beta-catenin signaling
- Authors
- Chen, Jing; Lee, Jaehoo; Bao, Cheng; Kim, Jin Tae; Lee, Hong Jin
- Issue Date
- Sep-2018
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- Breast cancer; beta-catenin; Cell cycle; Glycogen synthase kinase-3 beta; Trihydroxyisoflaovone
- Citation
- JOURNAL OF FUNCTIONAL FOODS, v.48, pp 498 - 506
- Pages
- 9
- Journal Title
- JOURNAL OF FUNCTIONAL FOODS
- Volume
- 48
- Start Page
- 498
- End Page
- 506
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/885
- DOI
- 10.1016/j.jff.2018.07.044
- ISSN
- 1756-4646
2214-9414
- Abstract
- The hepatic metabolites of daidzein has been demonstrated to be more potent in chronic diseases than daidzein. However, the investigation of their roles in estrogen receptor (ER)-negative breast cancer is limited. Here, the hepatic metabolite of daidzein 6,7,4'-trihydroxyisoflavone inhibited cell proliferation, induced cell cycle arrest at G2/M phase, and regulated the expression of cyclin B, cyclin dependent kinase (CDK)-1 and CDK2 in MCF10DCIS.com ER-negative breast cancer cells. 6,7,4'-Trihydroxyisoflavone activated glycogen synthase kinase (GSK)-3 beta, and suppressed the nuclear translocation of beta-catenin. Inhibition of GSK3 beta by lithium chloride reversed the effect of 6,7,4'-trihydroxyisoflavone on beta-catenin localization, CDK1, CDK2 and cyclin B expression, and the proliferation of MCF10DCIS.com. In xenograft animal model, 6,7,4'-trihydroxyisoflavone inhibited tumor growth, and regulated GSK3 beta phosphorylation and beta-catenin nuclear localization. These results indicate that 6,7,4'-trihydroxyisoflavone suppressed ER-negative breast cancer growth through regulating GSK3 beta/beta-catenin signaling, and 6,7,4'-trihydroxyisoflavone may be a potent chemopreventive agent in regulating the ER negative human mammary carcinogenesis.
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