Methylation of estrogen receptor-beta promoter 0N CpG sites in LNCaP cells

CHED 1310

Joshua B. Elston, joelston@transy.edu1, Xiang Zhang2, Yuet-Kin Leung2, and Shuk-mei Ho2. (1) Division of Natural Sciences and Mathematics, Transylvania University, 300 North Broadway, Lexington, KY 40508, (2) Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH 45267
Studies have shown that estrogen receptor-beta (ERb) acts as a tumor suppressor gene in prostate cancer (PCa). In higher grades of PCa, ERb expression disappears with no causal genetic mutation, rather, gene silencing is performed by CpG methylation in the promoter 0N region of ERb. Using a demethylation agent (5-aza-2'-deoxycytidine), we have analyzed by DNA sequencing/alignment that critical CpG centers are preferentially demethylated for a given concentration of demethylation agent. Ultimately, it was shown through Real Time RT-PCR that preferential demethylation at these critical CpG centers reactivate expression of ERb in LNCaP cells. This has prompted further studies into the binding capabilities of transcription factors at these critical sites for gene regulation. If discovered, a transcription factor's ability to bind to the promoter 0N region could serve as the master switch in ERb transcription.
 

Undergraduate Research Poster Session: Medicinal
2:00 PM-4:00 PM, Monday, March 26, 2007 Hyatt Regency Chicago -- Riverside Center, Poster

Division of Chemical Education

The 233rd ACS National Meeting, Chicago, IL, March 25-29, 2007