Natural and Synthetic Estrogens in Chronic Inflammation and Breast Cancer

Abstract

The oncogenic role of estrogen receptor (ER) signaling in breast cancer has long been established. Interaction of estrogen with estrogen receptor (ER) in the nucleus activates genomic pathways of estrogen signaling. In contrast, estrogen interaction with the cell membrane-bound G-protein-coupled estrogen receptor (GPER) activates the rapid receptor-mediated signaling transduction cascades. Aberrant estrogen signaling enhances mammary epithelial cell proliferation, survival, and angiogenesis, hence is an important step towards breast cancer initiation and progression. Meanwhile, a growing number of studies also provide evidence for estrogen’s pro- or anti-inflammatory roles. As other articles in this issue cover classic ER and GPER signaling mediated by estrogen, this review will discuss the crucial mechanisms by which estrogen signaling influences chronic inflammation and how that is involved in breast cancer. Xenoestrogens acquired from plant diet or exposure to industrial products constantly interact with and alter innate estrogen signaling at various levels. As such, they can modulate chronic inflammation and breast cancer development. Natural xenoestrogens generally have anti-inflammatory properties, which is consistent with their chemoprotective role in breast cancer. In contrast, synthetic xenoestrogens are proinflammatory and carcinogenic compounds that can increase the risk of breast cancer. This article also highlights important xenoestrogens with a particular focus on their role in inflammation and breast cancer. Improved understanding of the complex relationship between estrogens, inflammation, and breast cancer will guide clinical research on agents that could advance breast cancer prevention and therapy.

Lacticaseibacillus rhamnosus Probio-M9-Driven Mouse Mammary Tumor-Inhibitory Effect Is Accompanied by Modulation of Host Gut Microbiota, Immunity, and Serum Metabolome

“…Changes in the tumor size of mice ( n = 12 per group) were measured by a digital vernier calipers at days 12, 14, 16, 18, 20, and 22. With the assumption that the tumor was an ellipsoid body, the tumor volume was calculated according to the formula: V (mm 3 ) = (L × W 2 )/2, where L and W were the length and width of the tumor mass [ 31 ]. At day 22, mice were sacrificed and dissected, and tumors developed in the mice were fixed.…”

Health consequences of exposure to aircraft contaminated air and fume events: a narrative review and medical protocol for the investigation of exposed aircrew and passengers

“…OP flame retardants may have effects on the oestrogen receptor, androgen receptor and glucocorticoid receptor [ 198 , 199 ], by enhancing or blocking the activity of the naturally occurring ligand, such as oestrogen or testosterone. As an example, TCP has endocrine disrupting effects via various hormone pathways including the oestrogen receptor [ 198 - 201 ], which is implicated in breast cancer [ 202 , 203 ]. Causal connection.…”

Single-Cell Transcription Mapping of Murine and Human Mammary Organoids Responses to Female Hormones

“…Moreover, our findings that estrogen-exclusive LHS cells are highly differentiated compared to untreated LHS cells indicate that hormone treatment could be promoting cellular maturation, in accordance with previous studies [ 4 ]. These mature LHS cells also displayed an activation of pathways associated with proliferation and inflammation, which have been previously linked to estrogen-mediated activation [ 69 ].…”