内分泌干扰物化合物对雌激素受体功能的染色质动态-猫眼课题宝

内分泌干扰物化合物对雌激素受体功能的染色质动态

批准号：

8616375

负责人：

Craig J Burd

金额：

$24.32万

依托单位：

OHIO STATE UNIVERSITY

依托单位国家：

美国

项目类别：

财政年份：

2013

资助国家：

美国

项目状态：

已结题

起止时间：

2013-04-01 至 2016-03-31

来源：

https://reporter.nih.gov/project-details/8616375

关键词：

Address Affect Animal Model Binding Biochemical Biological Breast Breast Cancer Cell Cancer Patient Cells Cessation of life Characteristics Chemicals Chromatin Chromatin Structure Data Development Diagnosis Disease Endocrine Disruptors Environmental Estrogen Epigenetic Process Estradiol Estrogen Antagonists Estrogen Receptors Estrogen Therapy Estrogen receptor positive Estrogens Event Exhibits Exposure to Formaldehyde Gene Expression Profile Gene Targeting Genetic Transcription Genistein Genomics Glucocorticoid Receptor Growth Histone Deacetylation Hyperplasia Individual Lesion Ligands Long-Term Effects Malignant Neoplasms Mammary Neoplasms Mission Modeling Modification Monitor National Institute of Environmental Health Sciences Nuclear Receptors Nuclear Translocation Nucleosomes Physiological Plants Play Positioning Attribute Receptor Activation Receptor Gene Recruitment Activity Regulation Regulatory Element Research Response Elements Risk Risk Factors Role Signal Transduction Techniques United States Woman Work bisphenol A chromatin modification endocrine disruptor exposure epigenome genome-wide high risk histone methyltransferase histone modification hormone therapy human disease in vivo insight malignant breast neoplasm postnatal prenatal programs receptor receptor function response tumorigenesis

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A woman's overall lifetime exposure to estrogen is a critical risk factor for the development of breast cancer. A number of environmental compounds, termed endocrine disrupting compounds (EDCs) have been shown to bind and activate the estrogen receptor and are thus implicated in breast cancer tumorigenesis. However, it has become clear that EDC activation of the estrogen receptor induces ligand-specific transcriptional programs. It is our hypothesis that chromatin structure is a key regulator of endocrine, disruptor action in breast cancer development and progression. In this proposal, we will use an unbiased genomic approach to characterize chromatin structure in breast cancer cells following treatment with bisphenol A and genistein. EDC responsive regions will be characterized for chromatin modifications and nucleosome positioning. Finally, the effects of long term exposure to both bisphenol A and genistein on estrogen receptor recruitment will be examined. These studies will clarify the mechanisms by which EDCs elicit specific transcriptional profiles in the breast.

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