Resveratrol and other dietary polyphenols are inhibitors of estrogen metabolism in human breast cancer cells

Poschner, Stefan; Maier‐Salamon, Alexandra; Thalhammer, Theresia; Jäger, Walter

doi:10.1016/j.jsbmb.2019.03.001

Cited by 51 publications

(34 citation statements)

References 101 publications

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“…The treatment effect depends on the RSV concentrations. Specifically, resveratrol of low dosage could stimulate the growth of ERα+ (estrogen receptor α positive) breast cancer cells, while it always acts as an inhibitor in ERα-(estrogen receptor α negative) breast cancer cells by acting as an estrogen-metabolizing inhibitor to affect the proliferation of different types of breast cancer cells [26]. Bove et al found that 30 µM RSV could completely inhibit the proliferation of 4T1 cells [27].…”

Section: Discussionmentioning

confidence: 99%

The Cytotoxicity Effect of Resveratrol: Cell Cycle Arrest and Induced Apoptosis of Breast Cancer 4T1 Cells

Liang

Zhu

et al. 2019

Toxins

128

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Resveratrol, a natural polyterpenoid, can scavenge reactive oxygen species in vivo to carry out the functions of antioxidation and antiaging. Resveratrol's anti-cancer capability has attracted widespread attention, but its molecular mechanism has not been systematically explained. In this study, by comparing the activity of normal cell lines and cancer cell lines after treating with resveratrol, it was found that resveratrol has more significant cytotoxicity in cancer cell lines. Resveratrol could play a toxic role through inducing apoptosis of the cancer cell in a timeand concentration-dependent manner. A total of 330 significantly differential genes were identified through large-scale transcriptome sequencing, among which 103 genes were upregulated and 227 genes were downregulated. Transcriptome and qRT-PCR data proved that a large number of genes related to cell cycle were differentially expressed after the treatment of resveratrol. The changes of cell cycle phases at different time points after treating with resveratrol were further detected, and it was found that the cells were arrested in the S phase because of the percentage of cells in S phase increased and cells in G1/G0 phase decreased. In conclusion, resveratrol can inhibit the proliferation of 4T1 cancer cells by inhibiting cell cycle and inducing apoptosis. Key Contribution:Resveratrol exerts a more obvious toxic effect on cancer cells to induce apoptosis in a time-and dose-dependent manner. RNA-seq was used to overall explore potential mechanisms from a transcriptional level.

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Section: Discussionmentioning

confidence: 99%

The Cytotoxicity Effect of Resveratrol: Cell Cycle Arrest and Induced Apoptosis of Breast Cancer 4T1 Cells

Liang

Zhu

et al. 2019

Toxins

128

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“…The intake of polyphenols from food or as a food supplement for the prevention of BC is actually controversial, as only high concentrations are able to inhibit the proliferation of ERα and ERα + BC cells, while lower concentrations can even stimulate the growth of ERα + cells (43). One of the polyphenols studied for its inhibitory effects on BC is carnosol.…”

Section: Breast Cancermentioning

confidence: 99%

Polyphenols in cancer prevention: New insights (Review)

et al. 2020

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A huge volume of literature data suggests that a diet rich in fruits and vegetables, mostly due to the contribution of natural polyphenols, could reduce the incidence of specific cancers. Resveratrol, epigallocatechin gallate and curcumin are among the most extensively studied polyphenols: The majority of the effects attributed to these compounds are linked to their antioxidant and anti-inflammatory properties. The multiple mechanisms involved include the modulation of molecular events and signaling pathways associated with cell survival, proliferation, differentiation, migration, angiogenesis, hormonal activities, detoxification enzymes and immune responses. Notwithstanding their promising role in cancer prevention and treatment, polyphenols often have a poor bioavailability when administered as pure active principles, representing an important limit to their use. However, the bioavailability and thus the efficacy of these compounds can be improved by their administration in combination with other phytochemicals, with anticancer drugs or in polyphenol-loaded nanotechnology-based delivery systems. The possibility of combining conventional drugs with polyphenols offers very valuable advantages, such as the building of more efficient anticancer therapies with less side-effects on the health of patients. The present review focuses on current knowledge regarding the interactions between natural polyphenols and cancer development in order to gain a clearer comprehension of the potential mechanisms through which individual foods and food components may be exploited to reduce cancer risk. Contents 1. Introduction 2. Literature search 3. Classification of polyphenols 4. Prostate cancer 5. Colon cancer 6. Breast cancer 7. Lung cancer 8. Bladder cancer 9. Skin cancer 10. Pancreatic cancer 11. Leukemia 12. Conclusion

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“…AhR agonist ligands can be divided into three categories; exogenous ligands, including clinically approved drugs and newly designed compounds; and endogenous ligands. Dietary ligands have also been well reported, primarily from the Brassica vegetable family, as well as resveratrol, found in the skin of grapes . As these express antagonistic activity, however, they will not be discussed here.…”

Section: Ahr Agonistsmentioning

confidence: 99%

The aryl hydrocarbon receptor (AhR) as a breast cancer drug target

Baker

Sakoff

McCluskey

2019

Medicinal Research Reviews

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Breast cancer is the most common cancer in women, with more than 1.7 million diagnoses worldwide per annum. Metastatic breast cancer remains incurable, and the presence of triplenegative phenotypes makes targeted treatment impossible. The aryl hydrocarbon receptor (AhR), most commonly associated with the metabolism of xenobiotic ligands, has emerged as a promising biological target for the treatment of this deadly disease. Ligands for the AhR can be classed as exogenous or endogenous and may have agonistic or antagonistic activity. It has been well reported that agonistic ligands may have potent and selective growth inhibition activity in a number of oncogenic cell lines, and one (aminoflavone) has progressed to phase I clinical trials for breast cancer sufferers. In this study, we examine the current state of the literature in this area and elucidate the promising advances that are being made in hijacking the cytosolic-to-nuclear pathway of the AhR for the possible future treatment of breast cancer. K E Y W O R D S aryl hydrocarbon receptor, breast cancer, cancer drugs Abbreviations: 3MC, 3-methylcholanthrene; AF, aminoflavone; AF-1, activation function domain 1; AF-2, activation function domain 2; AhR, aryl hydrocarbon receptor; AhRR, aryl hydrocarbon receptor repressor; AIP, aryl hydrocarbon receptor-interacting protein; ANI-7, (Z)-2-(3,4-dichlorophenyl)-3-(1H-pyrrol-2-yl)acrylonitrile; ARNT, aryl hydrocarbon receptor nuclear translocator; BaP, benzo[a]pyrene; BE, botanical estrogen; bHLH, basic helixloop-helix; βNF, β-naphthoflavone; BRCA1, breast cancer susceptibility gene 1; BRCA2, breast cancer susceptibility gene 2; DNF, dinaphtho[1,2-b;1′2'-d] furan; ER, estrogen receptor; FDA, US Food and Drug Administration; FICZ, 6-formylindolo[3,2-b]carbazole; HAHs, halogenated aromatic hydrocarbons; HER-2, human epidermal growth factor receptor 2; HR, hormone receptor; Hsp90, heat shock protein 90; ITE, 2-(1′H-indole-3′-carbonyl)-thiazole-4carboxylic acid ester; LBD, ligand-binding domain; NLS, nuclear localization sequences; NSAID, nonsteroidal anti-inflammatory drug; p23, prostaglandin E synthase 3; PAHs, polycyclic aromatic hydrocarbons; PAS, period-aryl hydrocarbon receptor nuclear translocator-single minded; PAS-A, period-aryl hydrocarbon receptor nuclear translocator-single minded domain A; PAS-B, period-aryl hydrocarbon receptor nuclear translocator-single minded domain B; PCB, 3,3′,4,4′,5-pentachlorobiphenyl; PPI, proton pump inhibitor; PR, progesterone receptor; PR-A, progesterone receptor form A; PR-B, progesterone receptor form B; PR-C, progesterone receptor form C; ROS, reductive oxidative species; SERMs, selective estrogen receptor modulators; SULT1A1, sulfotransferase 1A1; TAD, transactivation domain; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDF, 2,3,7,8-tetrachlorodibenzofuran; TNBC, triplenegative breast cancer; Tregs, regulatory T cells; XAP-2, hepatitis B virus X-associated protein 2; XRE, xenobiotic response element. | BREAST CANCER BACKGROUNDBreast cancer is the most common cancer in women. Of...

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Resveratrol and other dietary polyphenols are inhibitors of estrogen metabolism in human breast cancer cells

Cited by 51 publications

References 101 publications

The Cytotoxicity Effect of Resveratrol: Cell Cycle Arrest and Induced Apoptosis of Breast Cancer 4T1 Cells

The Cytotoxicity Effect of Resveratrol: Cell Cycle Arrest and Induced Apoptosis of Breast Cancer 4T1 Cells

Polyphenols in cancer prevention: New insights (Review)

The aryl hydrocarbon receptor (AhR) as a breast cancer drug target

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