Examination of the Role of DNA Methylation Changes in Prostate Cancer using the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) Model

Abstract

We have previously shown that Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) tumors display altered DNA methyltransferase (Dnmt) expression and DNA methylation patterns, such that global DNA hypomethylation occurs early, while locus specific DNA hypermethylation occurs late during TRAMP tumor progression. In addition, we have identified several genes (Gsts, Mgmt, Pdlim4, and Zfp185), that are commonly silenced by promoter hypermethylation in human prostate cancer, that are also downregulated in TRAMP tumors. However, in TRAMP these genes do not display promoter hypermethylation. Although further studies suggest that other epigenetic mechanisms may be playing a role in the transcriptional regulation of these genes. Using a TRAMP Dnmt1 hypomorphic mouse model, we have tested the role of Dnmt1 in prostate cancer progression. At an early time point hypomorphic mice display advanced tumor progression and at a later time point hypomorphic mice have repressed tumor progression and metastases. These results suggest that both global hypomethylation and locus specific hypermethylation are important events during TRAMP tumorigenesis. This indicates a dual role for Dnmt1 in TRAMP tumor progression with a suppressive role in early stage disease and oncogenic role at later stages.

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Document Details

Document Type
Technical Report
Publication Date
Mar 01, 2009
Accession Number
ADA502739

Entities

People

  • Shannon R. Kinney

Organizations

  • Roswell Park Comprehensive Cancer Center

Tags

DTIC Thesaurus Topics

  • Adenocarcinoma
  • Biomedical Research
  • Body Weight
  • Cancer
  • Carcinoma
  • Correlation Analysis
  • Disease Attributes
  • Diseases And Disorders
  • Genes
  • Genetics
  • Methylation
  • Neoplasms
  • Prostate
  • Prostate Cancer
  • Statistical Analysis
  • Therapy
  • Tissues

Fields of Study

  • Biology

Readers

  • Molecular and genetic basis of cancer.
  • Prostate Cancer Biology.