Stop eating plastic, molecular signaling of bisphenol A in breast cancer

Environ Sci Pollut Res Int. 2018 Aug;25(24):23624-23630. doi: 10.1007/s11356-018-2540-y. Epub 2018 Jun 29.

Abstract

Breast cancer is the second most common fatal cancer in women. Developing a breast cancer is a multi-factorial and hormonal-dependent process, which may be triggered by many risk factors. An endocrine disrupting substance known as bisphenol A (BPA), that is used greatly in the manufacture of plastic products, was suggested as a possible risk factor for developing breast cancer. BPA has a strong binding affinity to non-classical membrane estrogen receptors like estrogen-related and G protein-coupled (GPER) receptors. Based on animal and in vitro studies, results showed a link between BPA exposure and increased incidence of breast cancer. BPA has the ability to alter multiple molecular pathways in cells namely, G protein-coupled receptor (GPER) pathway, estrogen-related receptor gamma (ERRγ) pathway, HOXB9 (homeobox-containing gene) pathway, bone morphogenetic protein 2 (BMP2) and (BMP4), immunoregulatory cytokine disturbance in the mammary gland, EGFR-STAT3 pathway, FOXA1 in ER-breast cancer cells, enhancer of zeste homolog 2 (EZH2), and epigenetic changes. Thus, the aforementioned alterations cause undesired gene stimulation or repression that increase risk of developing breast cancer. So, restricting exposure to BPA should be considered to aid in lowering the risk of developing breast cancer.

Keywords: Bisphenol A; Breast cancer; Molecular signaling; Plastics.

Publication types

  • Review

MeSH terms

  • Animals
  • Benzhydryl Compounds / metabolism
  • Benzhydryl Compounds / toxicity*
  • Breast Neoplasms / chemically induced*
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Cytokines / metabolism
  • Endocrine Disruptors / metabolism
  • Endocrine Disruptors / toxicity*
  • Enhancer of Zeste Homolog 2 Protein / metabolism
  • Environmental Exposure / adverse effects
  • Environmental Pollutants / metabolism
  • Environmental Pollutants / toxicity*
  • Epigenesis, Genetic
  • Female
  • Hepatocyte Nuclear Factor 3-alpha / genetics
  • Hepatocyte Nuclear Factor 3-alpha / metabolism
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / metabolism
  • Humans
  • Phenols / metabolism
  • Phenols / toxicity*
  • Plastics / chemistry
  • Receptors, Estrogen / metabolism
  • Receptors, G-Protein-Coupled / metabolism
  • Signal Transduction / drug effects

Substances

  • Benzhydryl Compounds
  • Cytokines
  • Endocrine Disruptors
  • Environmental Pollutants
  • FOXA1 protein, human
  • GPER1 protein, human
  • HOXB9 protein, human
  • Hepatocyte Nuclear Factor 3-alpha
  • Homeodomain Proteins
  • Phenols
  • Plastics
  • Receptors, Estrogen
  • Receptors, G-Protein-Coupled
  • EZH2 protein, human
  • Enhancer of Zeste Homolog 2 Protein
  • bisphenol A