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Florian CP, Mansfield SR, Schroeder JR. Differences in GPR30 Regulation by Chlorotriazine Herbicides in Human Breast Cells. Biochem Res Int. 2016;2016:2984081doi: 10.1155/2016/2984081.
Florian, C. P., Mansfield, S. R., & Schroeder, J. R. (2016). Differences in GPR30 Regulation by Chlorotriazine Herbicides in Human Breast Cells. Biochemistry research international, 20162984081. https://doi.org/10.1155/2016/2984081
Florian, Colin P, et al. "Differences in GPR30 Regulation by Chlorotriazine Herbicides in Human Breast Cells." Biochemistry research international vol. 2016 (2016): 2984081. doi: https://doi.org/10.1155/2016/2984081
Florian CP, Mansfield SR, Schroeder JR. Differences in GPR30 Regulation by Chlorotriazine Herbicides in Human Breast Cells. Biochem Res Int. 2016;2016:2984081. doi: 10.1155/2016/2984081. Epub 2016 Feb 03. PMID: 26955487; PMCID: PMC4756223.
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Biochem Res Int. 2016;2016:2984081. doi: 10.1155/2016/2984081. Epub 2016 Feb 03.

Differences in GPR30 Regulation by Chlorotriazine Herbicides in Human Breast Cells.

Biochemistry research international

Colin P Florian, Shelly R Mansfield, Jennifer R Schroeder

Affiliations

  1. Department of Biology, Millikin University, Decatur, IL 62522, USA.

PMID: 26955487 PMCID: PMC4756223 DOI: 10.1155/2016/2984081

Abstract

Over 200,000 cases of invasive breast cancer are diagnosed annually; herbicide contaminants in local water sources may contribute to the growth of these cancers. GPR30, a G protein coupled receptor, was identified as a potential orphan receptor that may interact with triazine herbicides such as atrazine, one of the most commonly utilized chlorotriazines in agricultural practices in the United States. Our goal was to identify whether chlorotriazines affected the expression of GPR30. Two breast cancer cell lines, MDA-MB-231 and MCF-7, as well as one normal breast cell line, MCF-10A, were treated with a 100-fold range of atrazine, cyanazine, or simazine, with levels flanking the EPA safe level for each compound. Using real-time PCR, we assessed changes in GPR30 mRNA compared to a GAPDH control. Our results indicate that GPR30 expression increased in breast cancer cells at levels lower than the US EPA drinking water contamination limit. During this treatment, the viability of cells was unaltered. In contrast, treatment with chlorotriazines reduced the expression of GPR30 in noncancerous MCF-10A cells. Thus, our results indicate that cell milieu and potential to metastasize may play a role in the extent of GPR30 response to pesticide exposure.

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