c-Met, a member of the tyrosine kinase family of proteins, is over-expressed in well-differentiated pancreatic endocrine neoplasms as well as many carcinomas including pancreatic, lung, breast, colorectal, head and neck, ovarian, renal, prostate, glioma, melanoma, gastric, hepatocellular, and a number of sarcomas. c-Met plays a role in several oncogenic pathways (PI3K-PDK1-AKT-mTor, Ras-Rac-Pak, Ras-Raf-MEK-ERK, and PLC-?) that regulate cell migration, invasion, angiogenesis, morphogenic differentiation, cell proliferation and survival. An underappreciated aspect of c-Met's role in oncogenesis is its potential exploitation in nanoparticle therapeutics. The external domain of c-Met provides a prime target for directing therapeutic nanoparticles to metastatic tumor cells. We have conjugated c-Met binding ligands to the surface of fluorescently labeled polymeric nanoparticles. Cells that exhibit low, medium, or high levels of c-Met expression were then exposed to our targeted particles where uptake was examined by flow cytometry and fluorescence microscopy. Details of the conjugation chemistry, characterization, and uptake studies will be discussed along with future opportunities.

c-Met: A new target for nanoparticle therapeutics

247th National Meeting (2014)

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