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Reprod Toxicol. 2015 Jul;54:136-40. doi: 10.1016/j.reprotox.2014.12.014. Epub 2014 Dec 29.

Hypothesis: Activation of rapid signaling by environmental estrogens and epigenetic reprogramming in breast cancer.

Author information

1
Center for Translational Cancer Research, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, TX, United States.
2
Center for Translational Cancer Research, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, TX, United States. Electronic address: cwalker@ibt.tamhsc.edu.

Abstract

Environmental and lifestyle factors are considered significant components of the increasing breast cancer risk in the last 50 years. Specifically, exposure to environmental endocrine disrupting compounds is correlated with cancer susceptibility in a variety of tissues. In both human and rodent models, the exposure to ubiquitous environmental estrogens during early life has been shown to disrupt normal mammary development and cause permanent adverse effects. Recent studies indicate that environmental estrogens not only have the ability to disrupt estrogen receptor (ER) signaling, but can also reprogram the epigenome by altering DNA and histone methylation through rapid, nongenomic ER actions. We have observed xenoestrogen-mediated activation of several nongenomic signaling pathways and have identified a target for epigenetic reprogramming in MCF-7 breast cancer cells. These observations, in addition to data from the literature, support the hypothesis that activation of rapid signaling by environmental estrogens can lead to epigenetic reprogramming and contribute to the progression of breast cancer.

KEYWORDS:

Breast cancer; Environmental estrogens; Epigenetics; Histone modifiers

PMID:
25554384
PMCID:
PMC4563990
DOI:
10.1016/j.reprotox.2014.12.014
[Indexed for MEDLINE]
Free PMC Article

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