Epigenetic Factors to Reduce Breast Cancer Risk – Part 6

Epigenetic Factors to Reduce Breast Cancer Risk – Part 6

In this 12-part series of articles, my primary goal is to empower you with information about the nutrients that can alter epigenetic factors to help you heal from breast cancer and to reduce your risk of recurrence.

For more information on my personal reasons for putting this information together, see Part 1 of the series.

This article, Part 6 of the series, shares the nutrients that have the ability to modify or restore receptors on the surface of breast cancer cells. The function of receptors on cells is to create a place for a chemical messenger (for instance, a hormone) to dock, which then allows the chemical messenger to direct the function of that particular cell.

65-70% of breast cancers are hormone receptor positive, meaning that the tumor cells have receptors to which estrogen can attach (known as “ER-positive”, or “ER+” breast cancer) and/or progesterone (known as “PR-positive” or “PR+” breast cancer). For these cancers, high levels of estrogen (and this includes xenoestrogens, or environmental estrogens) can promote the growth and spread of these tumor cells. Estrogen exerts many of its effects through two different estrogen receptors, estrogen receptor alpha, thought to lead to the proliferation of breast cells, and estrogen receptor beta, thought to oppose or reverse proliferation of breast cells.

Around 20% of hormone receptor positive breast cancer tumors also overexpress a protein known as human epidermal growth factor receptor 2 (“HER2″), which can make this type of breast cancer more aggressive.

15-25% of breast cancer tumors, however, display no hormone receptors or HER2 overexpression, this type is called “triple negative breast cancer” (or “TNBC”). TNBC can be more problematic to treat because all of the therapies developed for hormone receptor positive breast cancer don’t work with this form of breast cancer.

But take heart. Hard-working researchers have been discovering epigenetic nutrients that can downregulate or restore receptors on breast tumor cells, making them more receptive to standard treatments, impairing their ability to receive growth signals, and promoting cancer cell death.

PART 6 – NUTRIENTS THAT ALTER OR RESTORE RECEPTORS ON BREAST CANCER CELLS

Alpha-linolenic acid (ALA) – a fatty acid from flaxseed. When ALA enters the cell membrane, it disrupts protein receptors such as HER2 and estrogen receptors, reducing their activity. [1], [2]

Broussoflavonol B – a phytochemical from the bark of the paper mulberry tree (Broussonetia papyrifera). It downregulates a variant of estrogen receptor (“ER”) alpha known as ERa36, highly expressed in TNBC, and inhibits the growth of ER negative (“ER-“) breast cancer cells. [3]

Caffeine and caffeic acid – from (preferably) organic coffee. Suppresses the growth of ER+ and ER- cells, reduces the risk of TNBC, and sensitizes receptors to Tamoxifen, a commonly prescribed hormonal therapy for ER+ breast cancer, and reduces breast cancer growth. [4], [5]

Curcumin – from the root of the herb turmeric, and also available in the form of supplements (choose the bio-available formulations, usually containing piperine which increases absorption). Curcumin downregulates the expression of ER alpha in ER+/PR+ breast cancer cells. [6]

Cyanadin-3-glucoside – an anthocyanin found in acai, amaranth, blackberries, blackcurrants, cherries, black rice, pistachio nuts, red beans. Downregulates a variant of estrogen receptor alpha known as ERa36, highly expressed in TNBC, and inhibits the growth of ER- breast cancer cells. [7]

DIM – di-indolyl-methane, from cruciferous vegetables, taken in supplement form. DIM activates ER beta target genes. [8]

Genistein – from soybeans. Reactivates ER alpha in ER- breast cancer, restores sensitivity to Tamoxifen in Tamoxifen-resistant cells. [9]

Green Tea Polyphenols – on its own and when combined with sulforaphane, reactivates estrogen receptor alpha in TNBC. [10], [11] In ER+/PR+ breast cancer, EGCG from green tea downregulates ER alpha and inhibits proliferation of these cells. [12]

Melatonin – a hormone produced primarily by the pineal gland, also found in bananas, barley, black rice, tart cherries, ginger, oats, walnuts, and in supplement form. Melatonin selectively neutralizes the effects of circulating estrogen on the breast and interferes with the activation of the estrogen receptor in ER+ breast cancer, thus behaving as a selective estrogen receptor modulator (SERM). It also regulates enzymes involved in the biosynthesis of estrogen in the body, thus behaving as a selective estrogen enzyme modulator (SEEM). [13], [14], [15]
Pomegranate – extracts from pomegranate bind to estrogen receptors and downregulate the estrogen response elements in breast cancer cells. [16]

Sulforaphane – from cruciferous vegetables. Reactivates estrogen receptor expression in ER- breast cancer, inhibits ER alpha in ER+/PR+ metastatic breast cancer cells. [17], [18]

THC (Tetrahydrocannabinol) – from cannabis. In ER+/PR+ breast cancer, THC upregulates ER beta and inhibits the expression ER alpha-regulated genes that promote proliferation. [19]

Please note that this is not an exhaustive list, there will be other nutrients that have this effect as well and as I come across the research, I will add it here.

IMPORTANT NOTE: Please do not attempt to heal cancer using only a few nutrients. Cancer is a complex disease and requires a multi-disciplinary approach to effectively beat it. It is best to work with an oncologist and/or integrative oncologist and/or oncology naturopath and/or functional medicine doctor for the best results.

For more information on other epigenetic factors that reduce breast cancer risk, please see
Part 1 nutrients that can control regulatory genes
Part 2 nutrients that can reduce damage to DNA
Part 3 nutrients that stop rapid proliferation of cells
Part 4 nutrients that ease cancer promoting inflammation
Part 5 nutrients that change malignant cells back into healthy cells

References:

[1] Effect of A-linolenic Acid on Growth of Breast Cancer Cells with Varying Receptor Expression and Estrogen Environments – https://tspace.library.utoronto.ca/bitstream/1807/43341/1/Wiggins_Ashleigh_KA_201311_MSc_Thesis.pdf

[2] a-Linolenic Acid Reduces Growth of Both Triple Negative and Luminal Breast Cancer Cells in High and Low Estrogen Environments – https://www.ncbi.nlm.nih.gov/pubmed/26134471

[3] A novel anticancer agent Broussoflavonol B downregulates estrogen receptor (ER)-a36 expression and inhibits growth of ER-negative breast cancer MDA-MB-231 cells – https://www.ncbi.nlm.nih.gov/pubmed/23769740

[4] Caffeine and Caffeic Acid Inhibit Growth and Modify Estrogen Receptor and Insulin-like Growth Factor I Receptor Levels in Human Breast Cancer – http://clincancerres.aacrjournals.org/content/21/8/1877.full

[5] Coffee Consumption Modifies Risk of Estrogen-receptor Negative Breast Cancer – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3218935/

[6] The Effects of Turmeric (Curcumin) on Tumor Suppressor Protein (P53) and Estrogen Receptor (ERa) in Breast Cancer Cells – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354546/

[7] Cyanidin-3-o-glucoside Directly Binds to ERa36 and Inhibits EGFR-positive Triple-negative Breast Cancer – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356596/

[8] Selective Activation of Estrogen Receptor-ß Target Genes by 3,3′-Diindolylmethane – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2850231/

[9] Epigenetic Reactivation of Estrogen Receptor-a (ERa) by Genistein Enhances Hormonal Therapy Sensitivity in ERa-negative Breast Cancer – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3577460/

[10] Bioactive Dietary Supplements Reactivate ER Expression in ER-Negative Breast Cancer Cells by Active Chromatin Modifications – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3360625/

[11] Synergistic Epigenetic Reactivation of Estrogen Receptor-a (ERa) by Combined Green Tea Polyphenol and Histone Deacetylase Inhibitor in ERa-negative Breast Cancer Cells – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967543/

[12] In Vitro Mechanism for Down-regulation of ER alpha Expression by Epigallocatechin Gallate in ER+/PR+ Human Breast Cancer Cells – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4642730/

[13] Selective Estrogen Enzyme Modulator Actions of Melatonin in Human Breast Cancer Cells – https://www.ncbi.nlm.nih.gov/pubmed/18298468/

[14] Estrogen-Signaling Pathway: a Link Between Breast Cancer and Melatonin Oncostatic Actions – https://www.ncbi.nlm.nih.gov/pubmed/16647824/

[15] Melatonin as a Selective Estrogen Enzyme Modulator – https://www.ncbi.nlm.nih.gov/pubmed/19075592

[16] Evidence of Pomegranate Methanolic Extract in Antagonizing the Endogenous Serm, 27-hydroxycholesterol – https://www.ncbi.nlm.nih.gov/pubmed/26756990

[17] Bioactive Dietary Supplements Reactivate ER Expression in ER-Negative Breast Cancer Cells by Active Chromatin Modifications – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3360625/

[18] Regulation of Estrogen Receptor Alpha Expression in Human Breast Cancer Cells by Sulforaphane – https://www.ncbi.nlm.nih.gov/pubmed/18602823

[19] D9-Tetrahydrocannabinol Disrupts Estrogen-Signaling through Up-Regulation of Estrogen Receptor ß (Erß) – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4018723/

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