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Cell Motility and Invasiveness of Neurotibromin-Deficient Neural Crest Cells and Malignant Triton Tumor Lines
Annual rept. 1 Oct 2001-30 Sep 2002
TEXAS UNIV HEALTH SCIENCE CENTER AT SANANTONIO
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Our purpose is to examine the role of the NF1 gene product, neurofibromin, in modulating the migratory and invasive properties of neural crest cells NCC and neural crest-derived sarcoma cells. As a negative regulator of Ras signaling, neurofibromin may influence the responses of NC-derived cells to growth factors and extracellular matrix ECM molecules that affect motility. We use embryonic NCC and NC-derived sarcoma lines isolated from cisNfl p53 mice to compare integrin ECM receptor expression patterns, ECM adhesion preferences, migration on ECM substrata, invasion through ECM barriers, and dispersal along NCC pathways in vivo for wild-type and neurofibromin-deficient cells. In the past year, we have completed studies on the invasiveness of branchial arch neural crest cells isolated from Nf1 1, 1-, and -- mouse embryos, and developed methods to examine invasiveness of neural crest-derived cells in the trigeminal ganglion. In addition, we characterized the effects of TGF-beta on the invasiveness and neural crest phenotype of cisNf1 p53 sarcoma cells. Our studies address two important questions 1 what molecules control the migration and localization of NCC in the embryo 2 which growth factor signaling pathways affect the invasiveness of NC-derived sarcoma cells
APPROVED FOR PUBLIC RELEASE