Investigation of the Candidate Tumor Supressor Gene prk in Prostate
Abstract
The development of prostate cancer is thought to be driven, at least in part, by the inactivation of as yet unknown tumor suppressor genes, which are manifested as sites of nonrandom allele loss. Thus, the identification and characterization of these genes is of utmost importance to the understanding of this clinical important malignancy. Our early studies have led to the identification and characterization of Prk, a gene coding for a cell cycle serine/threonine kinase. We have mapped the Prk gene to chromosome 8p21, a site frequently lost in prostate cancer and proposed to harbor tumor suppressors. We have shown that the Prk gene is partially deleted in LACP9AD (pro static carcinoma), Weri-RB1 (retinoblastoma) and Dami (leukemia) cell lines. Prk gene expression, as detected by Northern blotting, is down-regulated in a majority of head and neck cancer. In addition, Prk protein interacts and phosphorylates Cdc25C, a dual specific phosphatase critical for the onset of mitosis. Our studies strongly suggest that a functional loss of Prk, a cell cycle regulator, may contribute to the development of various malignancies including prostate cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 2000
- Accession Number
- ADA385634
Entities
People
- David Dai
Organizations
- University of Cincinnati