<p>Tumor metastasis remains a leading cause of mortality in cancer patients. The epithelial-mesenchymal transition (EMT) is pivotal for the invasion and metastasis of cancer cells, facilitating the transformation from epithelial to mesenchymal phenotypes and thereby altering cellular morphology and function. SUMOylation, a critical post-translational modification, orchestrates a myriad of cellular physiological responses by binding to lysine residues on target substrates. This review delineates the signaling pathways of EMT, the mechanism of SUMOylation, and its consequential impact on the EMT process. Insight into the intricate regulation of SUMOylation within the EMT pathway could unlock novel avenues for the development and optimization of targeted EMT inhibitors that are dependent on SUMOylation modulation. This could potentially offer significant advances in the therapeutic strategies against cancer metastasis.</p>