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Metastasis is a leading cause of mortality in breast cancer and is critically influenced by cell–extracellular matrix (ECM) interactions, mechanical forces, and cellular motility. In this study, we present a cell surface engineering approach using tris(2-carboxyethyl)phosphine (TCEP), a biocompatible thiol-modifying agent, to modulate the biomechanical behavior of breast cancer cells. TCEP treatment increased surface thiol availability, enhanced phosphorylation of focal adhesion kinase (FAK), and promoted the elongation of pFAK-positive focal adhesions, along with cytoskeletal remodeling and stronger cell–ECM adhesion. These molecular and structural changes corresponded with significantly reduced migration and invasion of MCF7 and MDA-MB-231 cells. Using traction force microscopy (TFM), we further observed increased intracellular tension and traction stress, providing quantitative insight into how surface modification regulates mechanotransduction. These findings highlight the potential of cell surface thiol engineering to control cancer cell adhesion and motility, providing a platform for future identification of clinically applicable redox-modulating agents. Graphical abstract TCEP-mediated surface thiol modulation enhances focal adhesion and mechanical force generation, thereby suppressing breast cancer cell migration and invasion. Treatment with the biocompatible reducing agent TCEP cleaves cell surface disulfide bonds, increasing free thiol groups and reinforcing focal adhesion structures via FAK phosphorylation and actin remodeling. This redox modulation elevates traction force and intracellular stress, ultimately impairing both single-cell and collective migration. These findings identify surface thiol redox balance as a critical regulator of adhesion dynamics and mechanotransduction in breast cancer cells.