To investigate whether these bortezomib-induced changes in the tubulin polymerization were mediated by phosphorylation of stathmin, we examined the tubulin polymerization in stable U266 clones that overexpressing WT stathmin and the phosphorylation site-deficient stathmin mutants S16A, S25A and S38A. As shown in Figure 5C , by comparing with U266 cells, overexpression of WT stathmin and phosphorylation site-deficient mutants resulted in a significant decrease in the percent of polymerized tubulin following treatment with bortezomib ( Fig. 5C and Table 1) .