Details

Autor(en) / Beteiligte

• Katchy, Anne C.
• Pinto, Caroline
• Bondesson, Maria
• Williams, Cecilia

Titel

Abstract 547: Mapping of estrogen receptor-dependent and independent signaling pathways for xeno- and phytoestrogens

Ist Teil von

• Cancer research (Chicago, Ill.), 2012-04, Vol.72 (8_Supplement), p.547-547

Erscheinungsjahr

2012

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• Abstract Xenoestrogens (e.g. bisphenol A) and phytoestrogens (isoflavones) are endocrine disrupting chemicals (EDC) that are capable of disrupting hormonal signaling in mammary and reproductive systems. These compounds are similar in structure to estrogen and bind to the estrogen receptors (ER). Estrogen receptors are involved in the regulation of cell cycle, proliferation, and apoptosis. It is likely that these compounds could affect the same biological processes or have their own subsets of target pathways. Here, we extensively identify target genes and signaling pathways for selected xeno- and phytoestrogens. Dose response curves for these compounds were measured using real-time PCR (RT-PCR) and transactivation assays of known estrogen target genes. Gene expression profilings for each EDC were performed on MCF-7 breast cancer cell lines using dual-color comparative array. Validations of array results were carried out using RT-PCR. Gene ontology and gene network mapping studies were done to identify the mechanism of action of these compounds. Non-ER mediated targets and the kinetics of each EDC were investigated in detail. Results show that many target genes regulated by bisphenol A and Genistein were involved in biological processes including cell cycle and proliferation, similar to that of estrogen. This contributes to an increased understanding of the mechanisms of EDC action, which may be implicated in development of diseases such as breast cancer and reproductive disorders, and would contribute to a more reliable risk assessment of different EDC compounds. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 547. doi:1538-7445.AM2012-547