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

Abstract

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.

Natural remedies for non‐steroidal anti‐inflammatory drug‐induced toxicity

“…Many natural compounds are found in daily food supplements that are known to reduce the complication of renal injury caused by oxidative stress (Bak et al, 2016). Dichlorvos, at the dose 7.2 mg kg À1 b.w.…”

Differential Gene Regulation and Tumor-Inhibitory Activities of Alpha-, Delta-, and Gamma-Tocopherols in Estrogen-Mediated Mammary Carcinogenesis

“…Dietary components and bioactive natural compounds have been reported to inhibit mammary carcinogenesis by reduction of estrogen-induced oxidative stress as well as downregulation of ER-mediated signaling (7). Tocopherols, members of the vitamin E family present in the diet, have been demonstrated to exert chemopreventive effects in preclinical models of ER positive breast cancer (8-12) as well as lung, colon and prostate cancers (13-16).…”

Apoptosis Induced by (−)-Epicatechin in Human Breast Cancer Cells is Mediated by Reactive Oxygen Species

“…Considering the differences in their gene expression patterns, these could determine a different action of (−)-epicatechin on MCF-7 and MDA-MB-231 cells, as has been reported for other flavonoids [33]. It was established that flavonoids have beneficial effects on estrogen-driven breast cancer, due its similitude in chemical structure to estrogen [34]. The ability to mimic estrogen could be one of the reasons why (−)-epicatechin displayed a cytotoxic effect in ER-positive MCF-7 cells; however, we observed that (−)-epicatechin showed similar effects on cell viability in MDA-MB-231 cells.…”