Knockdown of Sec6 improves cell–cell adhesion by increasing α-E-catenin in oral cancer cells

The Sec6/8 complex is essential for specific exocytic sites on the plasma membrane and contributes to membrane growth in mammalian cells. In Madin-Darby canine kidney (MDCK) cells, E-cadherin and nectin-based adhesion complexes recruit the Sec6/8 complex to intercellular contacts. However, in cancer cells, the relationship between the Sec6/8 complex and the cell–cell adhesion proteins remains obscure. We demonstrate that the expression of α-E-catenin is increased by Sec6 siRNAs, and E-cadherin and β-catenin localize mainly at the cell–cell contact region in HSC3 cells, which were transfected with Sec6 siRNA.

► Knockdown of Sec6 suppresses wound healing in HSC3 cells.
► α-E-catenin increases by knockdown of Sec6 in HSC3 cells.
► Knockdown of Sec6 promotes the localization of E-cadherin and β-catenin to the cell–cell contact region.
► Knockdown of Sec8 downregulates Sec6 and increases α-E-catenin in HSC3 cells.