Research Paper Volume 11, Issue 18 pp 7817—7829

PRL-3 exerts oncogenic functions in myeloid leukemia cells via aberrant dephosphorylation of stathmin and activation of STAT3 signaling

Figure 6. Suggested mechanisms for a possible interplay between PRL-3, stathmin, and STATs. With blocking of PRL-3, expression and activity of stathmin is reduced, and STAT3 and STAT5 activity are suppressed in K562 cells. The proliferation, migration, and invasion are reduced. In contrast, expression and activity of stathmin is not altered with shPRL-3 in K562/G01 cells, which results in K562/G01 cells maintaining malignant phenotypes.