PTPu Regulates Cell Adhesion and Signaling in Human Prostate Cancer Cells
Abstract
The purpose of this research is to understand how cell adhesion-induced signals are transduced to negatively regulate cell growth and how this process is altered in prostate cancer. Extracellular events that regulate cell growth are transmitted by changes in tyrosine phosphorylation, which is controlled by protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs). Cancer causing genes encode PTKs that cause uncontrolled cell growth suggesting that PTPs play a role in negative growth regulation or function as tumor suppressors. Both cell adhesion molecules and tyrosine phosphorylation regulate contact inhibition of growth, i.e. when normal cells stop growing because they contact adjacent cells. Prostate cancer cells have defects in both cell adhesion and contact inhibition of growth. The receptor PTP, PTP mu, directly interacts with E-cadherin, the major cell-cell adhesion molecule in prostate cells. Loss of components of the cadherin pathway has previously been observed in prostate cancer cells. We recently demonstrated that PTPmu is no longer expressed in prostate cancer cells. Re-expression of PTPmu restores adhesion and negatively regulates cell growth. A detailed analysis of how PTPmu alters adhesion, cell growth and signal transduction is described and provides insights into both normal cell growth as well as malignant transformation in prostate cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 01, 2000
- Accession Number
- ADA392053
Entities
People
- Susann-brady Kalnay
Organizations
- Case Western Reserve University