Schisandrol A Exhibits Estrogenic Activity via Estrogen Receptor alpha-Dependent Signaling Pathway in Estrogen Receptor-Positive Breast Cancer Cells
- Authors
- Lee, Dahae; Kim, Young-Mi; Chin, Young-Won; Kang, Ki Sung
- Issue Date
- Jul-2021
- Publisher
- MDPI
- Keywords
- phytoestrogens; estrogen receptor; schisandrol A
- Citation
- PHARMACEUTICS, v.13, no.7
- Journal Title
- PHARMACEUTICS
- Volume
- 13
- Number
- 7
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/81776
- DOI
- 10.3390/pharmaceutics13071082
- ISSN
- 1999-4923
- Abstract
- The aim of this study was to examine the estrogen-like effects of gentiopicroside, macelignan, gamma-mangostin, and three lignans (schisandrol A, schisandrol B, and schisandrin C), and their possible mechanism of action. Their effects on the proliferation of the estrogen receptor (ER)-positive breast cancer cell line (MCF-7) were evaluated using Ez-Cytox reagents. The expression of extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (PI3K), AKT, and estrogen receptor alpha (ER alpha) was measured by performing Western blot analysis. 17 beta-estradiol (E2), also known as estradiol, is an estrogen steroid and was used as a positive control. ICI 182,780 (ICI), an ER antagonist, was used to block the ER function. Our results showed that, except for gentiopicroside, all the compounds promoted proliferation of MCF-7 cells, with schisandrol A being the most effective; this effect was better than that of E2 and was mitigated by ICI. Consistently, the expression of ERK, PI3K, AKT, and ER alpha increased following treatment with schisandrol A; this effect was slightly better than that of E2 and was mitigated by ICI. Taken together, the ER alpha induction via the PI3K/AKT and ERK signaling pathways may be a potential mechanism underlying the estrogen-like effects of schisandrol A. This study provides an experimental basis for the application of schisandrol A as a phytoestrogen for the prevention of menopausal symptoms.
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