Angiogenesis, the formation of new blood vessels, is a basic biological process that can be present in both physiological and clinical conditions such as wound healing or cancer cell metastasis. This process consists of a sequence of events including endothelial cell proliferation, migration and invasion, that culminate in new blood vessel formation. Proinflammatory prostaglandin E2 (PGE2) has been found to promote angiogenesis through endothelial cell migration and tube formation. PGE2 signaling is conveyed and regulated by its cognate receptors EP1, EP2, EP3 and EP4, their effector heterotrimeric G proteins and regulatory Arrestin proteins. The goal of this research project is to identify which molecules are involved in the PGE2 signaling pathways that lead to endothelial cell invasion, with special emphasis in G protein and Arrestin effectors. Transwell invasion assays will be used to examine the effects of PGE2 mimetics and inhibitors (in the form of EP ligand agonists and antagonists) as well as the effects of altering expression levels of EP effector molecules. The expression of proteins will be knocked down by transfecting cells with specific siRNAs and the gene specific knockdown effect on endothelial cell invasion will be examined. Real-time Polymerase Chain Reaction and Western blotting techniques will be employed to confirm the gene expression. It is well established that cancer progress depends on angiogenesis. Information concerning the mechanism of PGE2 induced invasion and angiogenesis would be beneficial to possible therapeutic techniques.