Tumor cells have to flexibly adapt to changing environmental conditions in order to successfully complete the invasion/metastasis cascade and to colonize a foreign tissue. The transcription factor SNAIL1 can trigger partial or complete epithelial-mesenchymal transition (EMT) which facilitates cellular plasticity and adaptation. Among other changes, EMT is accompanied by cell cycle arrest, increased motility, invasiveness, survival and therapy resistance. However, the molecular basis for SNAIL1-induced changes in tumor cell properties is not fully understood. Time-resolved transcriptome analyses in a colorectal cancer model for EMT provided evidence that upregulation of SNAIL1 leads to alteration and repurposing of Wnt/β-catenin and BMP pathway activity. Therefore, as working-hypothesis we suggest that SNAIL1 hijacks the activities of these two pathways for the execution of the EMT program. Accordingly, we will use complementary approaches of overexpression and CRISPR/Cas9-mediated loss-of-function in colorectal cancer cell lines and a mini-gut model for stepwise intestinal tumorigenesis to determine the role of the HMG-box transcription factor LEF1 in redirecting Wnt/β-catenin pathway activity towards anti-proliferative, pro-migratory gene expression. Likewise, we will investigate the importance of autocrine and paracrine BMP signaling for SNAIL1-induced cell motility and invasion, and its impact on reciprocal communication among epithelial and mesenchymal cells. Finally, to gain insight into pathway connectivity, we will probe for mutual dependence of Wnt/β-catenin and BMP signaling in the course of SNAIL1-induced EMT. Overall, these investigations are expected to yield an integrative model for the role of Wnt/β-catenin and BMP signaling and their downstream targets in colorectal cancer invasion and metastasis.