The ability of a cell to alter its adhesion properties is central for morphogenetic processes in development and it underlies the metastatic behaviour of cancer cells. The attachment and migration of cells is controlled through cell−matrix contacts, such as focal and fibrillary adhesions. Still, little is known about how adhesion plasticity is regulated. On page 2172 in this issue, Guido Posern and colleagues use a subclone of breast carcinoma cells grown in suspension to study the differences in non-adhesive versus adhesive cells in culture. The authors show that the cytoskeletal focal adhesion protein tensin3 (Tns3) is strongly downregulated on mRNA and protein levels when cells are grown in suspension. Likewise, transient non-adhering conditions for these cells cause a reduction in Tns3 expression, whereas the re-establishment of adhesion subsequently restores Tns3 levels. Further, the knockdown of Tns3 in the parental carcinoma cell line impairs cell migration and focal adhesion remodelling during cell spreading. Importantly, overexpression of Tns3 in non-adherent cells in suspension partially restores cell adhesion and the composition of focal contacts. The work demonstrates a link between Tns3 at cell-matrix contacts and its regulation by and contribution to the control of adhesion plasticity of breast carcinoma cells.
