A Novel Mechanism of Estrogen Action in Breast Cancer Cells Mediated Through ER-FE65 Complex Formation
Abstract
Fe65 is a multidomain adaptor protein with established functions in neuronal cells and neurodegeneration diseases [1]. It forms a multimeric complex with A amyloid precursor protein (APP) and histone acetyl transferase Tip60 to regulate the expression of genes [2]. Our published studies showed that Fe65 formed a complex with estrogen receptor (ER ), which permits estrogen (E2) protection of neuronal cell from apoptosis induced by the APP-Tip60 transcriptional complex [3]. Unpublished studies produced preliminary evidences for the expression of a Fe65 isoform in breast epithelial cells as well as evidences for its overexpression in human breast tumors. Although Tip60 is a tumor suppressor that sensitizes cellular response to DNA damage [4, 5], Fe65-null MEFs were found to be more sensitive to DNA damage induced cell death [6], suggesting that Fe65 may oppose Tip60 activity in DNA repair. Furthermore, estrogens (E2) were shown to protect MCF-7 breast cancer (BCa) cells from DNA damage-induced apoptosis [7].
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 2013
- Accession Number
- ADA581468
Entities
People
- Wenlong Bai
Organizations
- University of South Florida