Fig. 7From: Phosphatase of regenerating liver-3 (PRL-3) is overexpressed in classical Hodgkin lymphoma and promotes survival and migrationSuggested mechanism for a possible interplay between PRL-3, IL-13 and STAT6. With PRL-3 present (left), autocrine stimulation of IL-13 activates STAT6 and proliferation. With blocking of PRL-3 (right), STAT6 activity is reduced. L1236 cells do not possess the ability to increase IL-13 secretion and proliferation is reduced. HDLM2 cells can increase IL-13 secretion followed by an increase of pSTAT6 and thereby maintain cell growthBack to article page