Impact of lower concentrations of phytoestrogens on the effects of estradiol in breast cancer cells

Fp, Chen; Mh, Chien; Chern, I. y-y.

doi:10.3109/13697137.2014.1001357

Cited by 13 publications

(18 citation statements)

References 30 publications

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“…Thus, the effects of phytoestrogens were mainly proven in human breast cancer cell lines. In addition to other studies, our previous study demonstrated that genistein, resveratrol and quercetin do not stimulate MCF‐7 breast cancer cells and may induce apoptosis even at low concentrations . However, cancers are well known for high heterogeneity .…”

Section: Discussionmentioning

confidence: 76%

“…The present study confirmed the apoptosis effects of these phytoestrogens at general physiological concentrations in primary breast cancer cells, as well as in breast cancer cell lines. Furthermore, these phytoestrogens also inhibit cell viability in primary breast cancer cells, which was not significant in MCF‐7 breast cancer cell lines …”

Section: Discussionmentioning

confidence: 96%

“…Thus, we hypothesized that the discrepancy of phytoestrogens’ protective effects on breast cancer survivors may be related to its interaction with the endogenous estrogen present in breast tissue, even in post‐menopausal women. Our previous study showed that the combination of E 2 and phytoestrogens at higher concentrations (≧10 −6 M) demonstrated a significant increase in MCF‐7 cell viability, whereas at the generally physiological levels (10 −7 M), these phytoestrogens exerted a significant protective effect by suppressing the breast cancer cell viability induced by E 2 . Miodini et al reported that quercetin (1 μM) and genistein (5 μM) efficiently and significantly ( P < 0.01) counteracted the stimulation by oestradiol on the growth of MCF‐7 cells .…”

Section: Discussionmentioning

confidence: 98%

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Effects of phytoestrogens on the activity and growth of primary breast cancer cells ex vivo

Chen

Chien

2019

J of Obstet and Gynaecol

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Aim To explore the ex vivo effects of phytoestrogens on primary human breast cancer cells. Methods Breast cancer cells were obtained from patients who underwent primary breast cancer surgery, which were treated with 10−8 M 17β‐estradiol (E2), one of three phytoestrogens (genistein, resveratrol and quercetin, 10−7 M), and a combination of E2 and one of the three phytoestrogens for 48 h. These cells were then extracted for viability and apoptosis assay. The proteins involved in the proliferative and apoptotic pathways were evaluated by western blot analysis. Results Human breast cancer cell viability was inhibited by all phytoestrogens but induced by E2 with or without phytoestrogen. Apoptotic cells, as well as the proteins involved in apoptotic pathway and estrogen receptor (ER) β, were significantly increased in the cells treated with phytoestrogen alone. The use of E2 with or without a phytoestrogen revealed completely opposite results. The proteins involved in the proliferative pathway and ER α expression were all increased in the cultures with E2 with or without phytoestrogens. Conclusion In the presence of E2, these phytoestrogens lose the effects of suppressing breast cancer cells; contrastingly, induce growth stimulatory effects by inhibiting apoptosis and stimulating proliferation in primary breast cancer cells. Thus, the effects of phytoestrogens on breast cancer should be considered as E2 still present in breast cancer tissue.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 98%

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Effects of phytoestrogens on the activity and growth of primary breast cancer cells ex vivo

Chen

Chien

2019

J of Obstet and Gynaecol

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“…ERα expression is significantly induced by E 2 regardless of the presence of these phytoestrogens, although resveratrol is reported to have estrogen‐like activity in a transcriptional assay in cells overexpressing ER . Genistein, resveratrol, and quercetin may stimulate the proliferation of breast cancer cells, even at low physiological concentrations (at concentrations ≥ 10 –6 M) when E 2 is present . Therefore, the conflicting results regarding the effects of phytoestrogens on breast cancer cells may be attributed to the endogenous estrogens present in breast tissue …”

Section: The Interactions Between Steroid Hormones and Resveratrolmentioning

confidence: 99%

Mechanisms of action of nonpeptide hormones on resveratrol‐induced antiproliferation of cancer cells

Lin

Hsieh

Cheng

et al. 2017

Annals of the New York Academy of Sciences

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Nonpeptide hormones, such as thyroid hormone, dihydrotestosterone, and estrogen, have been shown to stimulate cancer proliferation via different mechanisms. Aside from their cytosolic or membrane-bound receptors, there are receptors on integrin α β for nonpeptide hormones. Interaction between hormones and integrin α β can induce signal transduction and eventually stimulate cancer cell proliferation. Resveratrol induces inducible COX-2-dependent antiproliferation via integrin α β . Resveratrol and hormone-induced signals are both transduced by activated extracellular-regulated kinases 1 and 2 (ERK1/2); however, hormones promote cell proliferation, while resveratrol induces antiproliferation in cancer cells. Hormones inhibit resveratrol-stimulated phosphorylation of p53 on Ser15, resveratrol-induced nuclear COX-2 accumulation, and formation of p53-COX-2 nuclear complexes. Subsequently, hormones impair resveratrol-induced COX-2-/p53-dependent gene expression. The inhibitory effects of hormones on resveratrol action can be blocked by different antagonists of specific nonpeptide hormone receptors but not integrin α β blockers. Results suggest that nonpeptide hormones inhibit resveratrol-induced antiproliferation in cancer cells downstream of the interaction between ligand and receptor and ERK1/2 activation to interfere with nuclear COX-2 accumulation. Thus, the surface receptor sites for resveratrol and nonpeptide hormones are distinct and can induce discrete ERK1/2-dependent downstream antiproliferation biological activities. It also indicates the complex pathways by which antiproliferation is induced by resveratrol in various physiological hormonal environments. .

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“…Among many bioactive natural compounds, genistein and resveratrol have been the most widely studied, and reports showed that both compounds inhibited estrogen-induced DNA synthesis and proliferation of ER-positive breast cancer cells [317–326]. However, genistein and resveratrol could differently modify ERE-dependent transcription and expression of ERE-mediated genes, such as ER, PR, and pS2/Trefoil factor 1(TFF1) in the presence and absence of estrogen [97, 270, 319, 324–327]. These effects of genistein and resveratrol could be mediated through both ER-dependent and ER-independent pathways.…”

Section: Bioactive Natural Products Targeting Estrogen-mediated Mementioning

confidence: 99%

Role of dietary bioactive natural products in estrogen receptor-positive breast cancer

Bak

Gupta

Wahler

et al. 2016

Seminars in Cancer Biology

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Estrogen receptor (ER)-positive breast cancer, including luminal-A and -B, is the most common type of breast cancer. Extended exposure to estrogen is associated with an increased risk of breast cancer. Both ER-dependent and ER-independent mechanisms have been implicated in estrogen-mediated carcinogenesis. The ER-dependent pathway involves cell growth and proliferation triggered by the binding of estrogen to the ER. The ER-independent mechanisms depend on the metabolism of estrogen to generate genotoxic metabolites, free radicals and reactive oxygen species to induce breast cancer. A better understanding of the mechanisms that drive ER-positive breast cancer will help optimize targeted approaches to prevent or treat breast cancer. A growing emphasis is being placed on alternative medicine and dietary approaches toward the prevention and treatment of breast cancer. Many natural products and bioactive compounds found in foods have been shown to inhibit breast carcinogenesis via inhibition of estrogen induced oxidative stress as well as ER signaling. This review summarizes the role of bioactive natural products that are involved in the prevention and treatment of estrogen-related and ER-positive breast cancer.

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Impact of lower concentrations of phytoestrogens on the effects of estradiol in breast cancer cells

Cited by 13 publications

References 30 publications

Effects of phytoestrogens on the activity and growth of primary breast cancer cells ex vivo

Effects of phytoestrogens on the activity and growth of primary breast cancer cells ex vivo

Mechanisms of action of nonpeptide hormones on resveratrol‐induced antiproliferation of cancer cells

Role of dietary bioactive natural products in estrogen receptor-positive breast cancer

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