In mammals, the same pathway is triggered by certain cytokines. Binding induces receptor dimerization, cross-phosphorylation of and by the receptor-bound JAK kinases, and docking and activation of STAT transcription factors. The pathway is constitutively activated in many human cancers, and Montell believes that the consequence may be increased migration, in addition to the previously noted effects on survival and proliferation.
This may be especially pertinent for the many cancers that are derived from normally stationary epithelial cells. In the flies, says Montell, “we're studying the conversion of epithelial cells to migratory cells, and this is something that characterizes metastasis.” Experiments are underway to test whether manipulation of the JAK/STAT pathway in ovarian carcinoma cells affects the cells' motility. ▪