Prostate Cancer Cell Growth: Stimulatory Role of Neurotensin And Mechanism of Inhibition by Flavonoids as Related to Protein Kinase C
Abstract
The purpose is to define the relationships between neurotensin (NT) and protein kinase C (PKC) isotypes and to investigate the mechanism by which flavonoids (FLAV) inhibit NT-induced signaling in PC3 cells. The long-range scope is to determine the significance of NT as a participant in the negative effects of high fat intake on PC incidence and growth, and the positive effects of diets containing large amounts of FLAV. Our results show that NTinduced growth signaling in PC3 cells involves and requires the activation of several PKC isotypes, that arachidonic acid release and lipoxygenase activity participate in the signaling process, that cellular metabolism and ATP levels are important inputs to NT receptor function, and that activated PKC feeds back to regulate the ability of NT receptor to bind and to initiate signaling. These findings have implications regarding general mechanisms of G protein-linked receptor function and the design of new agents to block NT-induced growth signaling in PC.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 2007
- Accession Number
- ADA468073
Entities
People
- Paul Dobner
- Robert E. Carraway
- Sazzad Hassan
Organizations
- University of Massachusetts Medical School