Epithelial-mesenchymal transition (EMT) occurs when individual epithelial cells detach from the epithelial tissue and then migrate to distant sites. This process occurs throughout development, where cells from primordial epithelial tissues are triggered to detach, migrate, and colonize distant locations to establish new tissues. This process is also a fundamental part of cancer metastasis of epithelial tumors. In development, EMT events are triggered by specific and carefully controlled signal transduction pathways, including signaling initiated by the c-met receptor tyrosine kinase. In addition to driving EMT, c-met signaling also activates cell proliferation and increased cell survival. Despite a potentially central role in cancer progression and other diseases, signaling downstream of c-met receptor is not well characterized and thus efforts to perturb c-met signaling during disease progression are hindered. Here we discuss recent advances in our molecular understanding of how c-met signaling is transduced, with an emphasis placed on reconstructing the architecture of the c-met signaling pathway at the molecular level.