Overexpressed or activated hepatocyte growth factor receptor, encoded by the MET proto-oncogene, was found in the majority of colorectal carcinomas (CRCs), whose stepwise progression to malignancy requires transcriptional activation of β-catenin. We here demonstrate that a functional crosstalk between Met and β-catenin signaling sustains and increases CRC cell invasive properties. Hepatocyte growth factor (HGF) stimulation prompts β-catenin tyrosine phosphorylation and dissociation from Met, and upregulates β-catenin expression via the phosphatidylinositol 3-kinase pathway in conditions that mimic those found by the invading and metastasizing cells. Additionally, a transcriptionally active form of β-catenin, known to be oncogenic, enhances Met expression. Furthermore, HGF treatment increases the activity of the β-catenin-regulated T-cell factor transcription factor in cells expressing the wild-type or the oncogenic β-catenin. In the mirror experiments, either Met or β-catenin knocking down also reduces their protein level. In biological assays, β-catenin knocking down abrogates the HGF-induced motile phenotype, whereas active β-catenin fosters ligand-independent cell scattering. Met and β-catenin also cooperate in promoting entry into the cell cycle and in protecting cells from apoptosis. In conclusion, Met and β-catenin pathways are mutually activated in CRC cells. This might generate a self-amplifying positive feedback loop resulting in the upregulation of the invasive growth properties of CRC cells.