Analysis of Morphogenic Effect of hDAB2IP on Prostate Cancer and its Disease Correlation
Abstract
It is known that prostate cancer (PCa) acquires its malignant phenotypes by losing the ability to differentiate into mature cells. Therefore, restoration of the normal differentiated phenotype in AIPCa certainly can suppress the progression of PCa, which offers a new therapeutic strategy for PCa treatment. Using molecular biologic approaches, our laboratory was able to unveil an altered genetic make-up that is involved in cell differentiation in normal prostatic epithelium. Data from our laboratory has documented the potential role of this novel gene, hDAB2IP, in the cell differentiation of normal prostatic epithelia. In PCa, hDAB2IP is often down regulated. Thus, we proposed to study the underlying mechanism leading to the loss of hDAB2IP gene expression. In addition to the genetic mutations of tumor suppressor genes associated with PCa, recent data clearly indicated that epigenetic alterations are also involved in this silencing. In this study, we have shown that both histone methylation and histone deacetylation play an important part in silencing hDAB2IP gene expression and this event is mediated by a poplycomb group transcription complex Ezh2. The outcome of this study provides a bettter understanding of the fundamental changes between normal prostatic basal/stem cell and AIPCa, and further lead to the development of a novel and more effective intervention for this disease.
Document Details
- Document Type
- Technical Report
- Publication Date
- Feb 01, 2005
- Accession Number
- ADA434489
Entities
People
- Jer-Tsong Hsieh
Organizations
- University of Texas at Dallas