A Mouse Model for Prostate Cancer
Abstract
Mouse models of carcinogenesis have provided significant insights into the molecular mechanisms of tumor suppressor gene function. Our goal is to develop mouse models that recapitulate early stages of prostate carcinoma. Using such models we have demonstrated that the Nkx3.1 homeobox gene represents a prostate-specific tumor suppressor that undergoes epigenetic inactivation through loss of protein expression. Loss-of-function of Nkx3.1 in mice results in histopathological defects that resembles prostate cancer initiation in humans, and cooperates with loss-of-function of the Pten tumor suppressor gene in cancer progression. Furthermore, our findings suggest that the molecular mechanisms that mediate this cooperativity include the synergistic activation of Akt (protein kinase B), a key modulator of cell growth and survival. We propose that interactions between tissue-specific regulators such as Nkx3.1 and broad-spectrum tumor suppressors such as Pten underlie the distinct phenotypes of different cancers.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2001
- Accession Number
- ADA398566
Entities
People
- Cory Abate-shen
Organizations
- Robert Wood Johnson Medical School