The hypothesis to be tested is that the a6 and its variant a6p the invasion of human laminin 5 and laminin 10/11 coated structures. The a6p variant on the cancer cells acts to preserve the intracellular structural and signaling features for migration and invasion. The a6p is proposed to arise by receptor processing on the cell surface. The adhesion properties of the tumor cells on laminin 5 and laminin 10/11 will be interrupted by peptides or small molecules. The following specific aims are proposed: 1. Determine the functional role of the a6pb1 or a6pb4 variants.
The aim i ncludes determining the distribution of the variants in the focal adhesion site or hemidesmosome respectively and alteration of cellular adhesion, migration or invasion on laminin 5 and laminin 10/11. 2. Determine whether the mechanism of a6p integrin production is due to receptor processing. 3. Determine if blocking cell adhesion by d-amino peptides or small molecules will alter the growth, invasion or the survival phenotype of human prostate cancer cells in culture, prostate cells in a human organ culture and or a prostate cancer xenograft.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA056666-10
Application #
7252055
Study Section
Subcommittee G - Education (NCI)
Project Start
Project End
Budget Start
2006-04-01
Budget End
2007-03-31
Support Year
10
Fiscal Year
2006
Total Cost
$123,550
Indirect Cost
Name
University of Arizona
Department
Type
DUNS #
806345617
City
Tucson
State
AZ
Country
United States
Zip Code
85721
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