Abstract A1-08: Comparative genomics study of FOXA/ER dual regulation in breast cancer and liver cancer

Abstract

Abstract Estrogen, the female dominant hormone, has been found to play critical roles in cancers for over 100 years. In 1896, estrogen was found to promote the tumor growth of breast cancer; and in 1937, estrogen was found to prevent the tumor growth of liver cancer. After the estrogen receptor alpha (ERα) was identified in 1958, ERα-mediated estrogen signaling was found to promote or prevent the growth of breast cancer cells or liver cancer cells, respectively. Recent studies showed that ERα-mediated estrogen signaling in promoting the growth of breast cancer cells was dependent of forkhead box protein A1 (FOXA1). Our recent study showed that ERα-mediated estrogen signaling in preventing the growth of liver cancer cells also depended on FOXA factors (FOXA1 and FOXA2). Thus, FOXA-dependent ERα-mediated estrogen signaling plays opposite roles in the growth of breast cancer and liver cancer cells. Here, we applied genomic approaches to identify 184 FOXA/ER dual target genes that showed opposite expression in response to estrogen-mediated stimulation or suppression of cell growth in breast or liver cancer cells. Gene ontology analysis showed that the majority of these FOXA/ER dual target genes were involved in the processes of cell proliferation and growth, cell death, tissue development, and cancer. Manipulations of the expression of these target genes were able to reverse the growth of breast and liver cancer cells. Thus, these 184 FOXA/ER dual target genes provide us a novel set of potential biomarkers and therapeutic targets for both breast cancer and liver cancer. Note: This abstract was not presented at the conference. Citation Format: Zhaoyu Li. Comparative genomics study of FOXA/ER dual regulation in breast cancer and liver cancer. [abstract]. In: Proceedings of the AACR Special Conference on Translation of the Cancer Genome; Feb 7-9, 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 1):Abstract nr A1-08.