FAK Signaling in the Acquisition of a Cancerous Phenotype in Breast Epithelial Cells
Abstract
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that localizes to focal adhesion. FAK works as a transducer of extracellular signals that enter the cell via the integrins. FAK has been found to play an important role in normal biological process, including focal adhesion turnover, spreading, motility, cell cycle progression and cell survival. Many of the cellular processes mediated by FAK are deregulated in cancer, including proliferation, survival, as well as motility and invasion, which are key steps in metastasis. FAK is found to be overexpressed in a variety of cancer cells and tumors, including breast cancer tumors. Furthermore, FAK expression correlates with highly motile cancer cells and tumor invasiveness. Since FAK is overexpressed in breast cancer, and it is a mediator of cell cycle progression, motility and survival, the role of increased FAK signaling in progression and/or acquisition of cancer phenotypes will be investigated. A breast cancer cell model system will be used to increase FAK signaling, by overexpression of wild type FAK or an activated FAK construct, SuperFAK, in normal breast epithelial cells. Conversely FAK signaling will be inhibited by expressing of a naturally occurring dominant negative FAK variant, FRNK, in breast cancer epithelial cells.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2001
- Accession Number
- ADA392563
Entities
People
- Michael D. Schaller
- Veronica Gabarra
Organizations
- University of North Carolina at Chapel Hill