Cellular Adhesion and Prostate Tumor Progression

University Of Arizona, Tucson AZ

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Abstract

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 includes 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.