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Review
. 2021 Mar 30;26(1):18-24.
doi: 10.15430/JCP.2021.26.1.18.

Understanding the Mechanistic Link between Bisphenol A and Cancer Stem Cells: A Cancer Prevention Perspective

Cassandra Winz  1   2 , Nanjoo Suh  1   3
Affiliations
Review

Understanding the Mechanistic Link between Bisphenol A and Cancer Stem Cells: A Cancer Prevention Perspective

Cassandra Winz et al. J Cancer Prev. .

Abstract

Endocrine disruptors, such as bisphenol A (BPA), have become more frequently present in the environment as contaminants, especially in industrialized countries. Long-term effects of these environmental contaminants in humans are elusive. With their structural similarity to estrogen, many environmental contaminants including BPA, have been shown to mimic the biological functions of estrogen, potentially contributing to the development of breast cancer. It has been well established that BPA exerts estrogenic activity in animal models and in vitro systems. There is a concern for adverse effects from the exposure to BPA in regard to developmental and reproductive toxicities. However, the mechanisms by which BPA promotes breast cancer development remain unknown. Understanding the role of endocrine disruptors and their key mechanisms of action is important for public health, especially by providing a foundation for a better intervention approach in cancer prevention.

Keywords: Breast cancer; Cancer stem cells; Endocrine disruptors; Estrogen receptor.

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Conflict of interest statement

CONFLICTS OF INTEREST No potential conflicts of interest were disclosed.

Figures

Figure 1
Figure 1. Chemical structures of estrogen and synthetic bisphenols.
Alternatives of bisphenol A (BPA), bisphenol AF (BPAF, hexafluorobisphenol A), bisphenol F (BPF), and bisphenol S (BPS), bisphenol B (BPB), and bisphenol AP (BPAP, 4,4′-[1-Phenylethylidene] bisphenol) are also shown.
Figure 2
Figure 2. Potential mechanisms of BPA-induced breast cancer development and progression.
BPA, bisphenol A; ERA, estrogen receptor alpha; GPR30, G-protein-coupled receptor 30; TET2, ten-eleven translocation 2; SNAIL, Snail family zinc finger protein; ERK1/2, extracellular signal-regulated kinase 1/2.
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