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 transducers extracellular signals to the inside of the cell. FAK mediates normal cellular processes including motility, survival, and cell cycle regulation. FAK is overexpressed in a variety of tumors. Wild type FAK and an activated mutant of FAK, SuperFAK, were expressed in the normal breast epithelial cell line, MCF10A, in order to enhance FAK signaling. The elevation of FAK signaling alone had no effect in the adhesion independent growth of the MCF10A cells. The addition of high levels of epidermal growth factor to FAK and SuperFAK expressing MCF10As lead to the formation of soft agar colonies. In the second model system, FAK was inhibited in a breast cancer epithelial cell line, T47D, using FRNK, a dominant negative variant of FAK. When FRNK was expressed in the T47D cancer cells, a loss in their adhesion independent growth was observed. The underlying mechanisms for some of the observed effects are being investigated. Similar effect of FAK signaling on tumorigenesis in vivo is apparent. The data indicates the potential importance of aberrant FAK signaling as a cause for some of the phenotypic changes that occur when a cell becomes oncogenically transformed.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2002
- Accession Number
- ADA405486
Entities
People
- Michael D. Schaller
- Veronica Gabarra-niecko
Organizations
- University of North Carolina at Chapel Hill