Effects of Estrogen Metabolite 2-Methoxyestradiol on Tumor Suppressor Protein p53 and Proliferation of Breast Cancer Cells

Siebert, Amy E; Sanchez, Amelita; Dinda, Sumi; Moudgil, Virinder K.

doi:10.3109/19396368.2011.633152

Cited by 18 publications

(24 citation statements)

References 63 publications

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“…Reports indicate that breast cancer cells treated with CUR show a significant downregulation in the expression of ERα compared with the control cells 40. Previous studies, including studies from our laboratory, have shown that treatment with estrogen in T-47D breast cancer cells causes increased cell proliferation and upregulation of the tumor suppressor protein, p53 47–49. In this study, we have analyzed the effects of CUR on the expression of ERα and p53 in the presence of estrogen, bisphenol-a (BPA), and anti-estrogens in T-47D breast cancer cells.…”

Section: Introductionmentioning

confidence: 84%

The effects of turmeric (curcumin) on tumor suppressor protein (p53) and estrogen receptor (ERα) in breast cancer cells

Hallman¹,

Aleck²,

Dwyer³

et al. 2017

BCTT

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Curcumin (CUR) is a compound that has antibacterial, antiviral, anti-inflammatory, and anticancer properties. In this study, we have analyzed the effects of CUR on the expression of ERα and p53 in the presence of hormones and anti-hormones in breast cancer cells. Cells were cultured in a medium containing charcoal-stripped fetal bovine serum to deplete any endogenous steroids and treated with CUR at varying concentrations or in combination with hormones and anti-hormones. Protein analysis revealed a relative decrease in the levels of p53 and ERα upon treatment with 5–60 µM CUR. In cell proliferation studies, CUR alone caused a 10-fold decrease compared with the treatment with estrogen, which suggests its antiproliferative effects. Delineating the role of CUR in the regulation of p53, ERα, and their mechanisms of action may be important in understanding the influence of CUR on tumor suppressors and hormone receptors in breast cancer.

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Section: Introductionmentioning

confidence: 84%

The effects of turmeric (curcumin) on tumor suppressor protein (p53) and estrogen receptor (ERα) in breast cancer cells

Hallman¹,

Aleck²,

Dwyer³

et al. 2017

BCTT

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“…ERα levels were normalized to protein levels of the evolutionarily conserved actin protein according to the manufacturer’s protocol. The protein bands were visualized using the Chemi-Doc imaging system (Bio-Rad) 4,19…”

Section: Methodsmentioning

confidence: 99%

“…The estrogen 17β-estradiol (E 2 ) is known to enhance cellular division in target cells by binding to its specific protein receptor called the estrogen receptor (ERα). Previous studies from our laboratory have shown the addition of E 2 to breast cancer cells causes a downregulation of the ERα and an increase in cellular proliferation 4. Phytoestrogens have been shown to bind to ER (α and β) and act as either ER antagonists or agonists 5.…”

Section: Introductionmentioning

confidence: 99%

The regulation of steroid receptors by epigallocatechin-3-gallate in breast cancer cells

Hallman¹,

Aleck²,

Quigley³

et al. 2017

BCTT

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It has been reported that phytoestrogen epigallocatechin gallate (EGCG) suppresses cancer cell proliferation and may have antitumor properties. In this study, we analyzed the effects of EGCG on estrogen receptor α (ERα) and progesterone receptor in hormone-dependent T-47D breast cancer cells. Western blot analysis revealed EGCG induced a concentration-dependent decrease in ERα protein levels, with a 56% reduction occurring with 60 µM EGCG when compared to controls. Downregulation of ERα protein levels was observed after 24-hour co-treatment of T-47D cells with 60 µM EGCG and 10 nM 17β-estradiol (E2). The proliferative effect of E2 on cell viability was reversed when treated in combination with EGCG. In contrast, the combination of EGCG with the pure ER antagonist, ICI 182, 780, showed no further reduction in cell number as only 5% of the cells were viable after 6 days of treatment. These studies may provide further understanding of the interactions among flavonoids and steroid receptors in breast cancer cells.

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“…Most experimental studies of estrogen metabolites that have been published have examined their actions on breast cancer, gynecological tumors, lipid metabolism, atherosclerosis, as well as on the function of VSMCs, CFs, or GMCs, whereas little information is available on hepatic fibrosis and HSCs [39][40][41][42]. HSCs are VSMC, CF, or GMC analogs and belong to the pericytes generically; thus, they may have many properties in common including a major role in fibrosis and similar reactions to E 2 .…”

Section: Estrogen Metabolitesmentioning

confidence: 99%

Estrogen derivatives

Zhang

Wu²

2013

European Journal of Gastroenterology & Hepatology

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Sex differences in the incidence of liver cirrhosis and portal hypertension have been reported by epidemiological studies. Previous studies have indicated that estrogen therapy improved hepatic fibrosis, inhibited the activation of hepatic stellate cells, and reduced portal pressure, whereas the administration of exogenous estrogens resulted in some potential risks, limiting their clinical use. However, the biological actions of estrogens are mediated by three subtypes of estrogen receptors (ERs): ERα, ERβ, and G-protein-coupled ER. These ER subtypes act in distinct ways and exert different biological effects that mediate genomic and nongenomic events, resulting in tissue-specific responses. In addition, active estrogen metabolites, with little or no affinity for ERs, could mediate the fibrosuppressive effect of estrogens through an ER-independent pathway. Taken together, such specific estrogen derivatives as ER selective agonists, or active estrogen metabolites, would provide novel therapeutic opportunities, stratifying this hormonal treatment, thereby reducing undesired side-effects in the treatment of liver cirrhosis and portal hypertension.

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Effects of Estrogen Metabolite 2-Methoxyestradiol on Tumor Suppressor Protein p53 and Proliferation of Breast Cancer Cells

Cited by 18 publications

References 63 publications

The effects of turmeric (curcumin) on tumor suppressor protein (p53) and estrogen receptor (ERα) in breast cancer cells

The effects of turmeric (curcumin) on tumor suppressor protein (p53) and estrogen receptor (ERα) in breast cancer cells

The regulation of steroid receptors by epigallocatechin-3-gallate in breast cancer cells

Estrogen derivatives

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Effects of Estrogen Metabolite 2-Methoxyestradiol on Tumor Suppressor Protein p53 and Proliferation of Breast Cancer Cells

Cited by 18 publications

References 63 publications

The effects of turmeric (curcumin) on tumor suppressor protein (p53) and estrogen receptor (ER&alpha;) in breast cancer cells

The effects of turmeric (curcumin) on tumor suppressor protein (p53) and estrogen receptor (ER&alpha;) in breast cancer cells

The regulation of steroid receptors by epigallocatechin-3-gallate in breast cancer cells

Estrogen derivatives

Contact Info

Product

Resources

About

The effects of turmeric (curcumin) on tumor suppressor protein (p53) and estrogen receptor (ERα) in breast cancer cells

The effects of turmeric (curcumin) on tumor suppressor protein (p53) and estrogen receptor (ERα) in breast cancer cells