Biomarkers of Selenium Chemoprevention of Prostate Cancer
Abstract
The purpose of the present study was to examine the mechanism of selenium growth inhibition in PC-3 human prostate cancer cells Selenium retarded cell cycle progression at multiple transition points without changing the proportion of cells in different phases of the cell cycle Selenium treatment also resulted in a marked induction of apoptosis. Array analysis was then applied to profile the gene expression changes mediating selenium-induced growth initiation A large number of potential selenium-responsive genes that are diverse in biological functions were identify. These genes fell into 12 clusters of distinct kinetics of modulation by selenium. The expression changes of 10 genes critically involved in cell cycle regulation were selected for verification by Western analysis. An agreement rate of 70% was obtained from these confirmation experiments. The array data enabled us to focus on the role of potential key genes (e.g., GADD153 CHK2, and p21WAFI) in initiating the action of selenium, as well as to propose tentative signaling pathways that are integral to the downstream effects of these genes The data also provide valuable insights into novel biological effects of selenium, such as inhibition of cell invasion, initiation of DNA repair, and induction of TGF-beta signaling.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 2003
- Accession Number
- ADA414866
Entities
People
- Yan Dong
Organizations
- Health Research, Incorporated