Paracrine signaling through the JAK/STAT pathway activates invasive behavior of ovarian epithelial cells in Drosophila (original) (raw)

ptosis and promote proliferation (Shen et al., 2001). Expression of a constitutively activated form of STAT3 in 293T cells results in increased expression of cyclin D1, BCL-XL, and c-myc, which promote cell cycle progression, cell survival, and proliferation, respectively. Inhibition of STAT3 in myeloma cells results in apoptosis (Catlett-Falcone et al., 1999b), and dominant-negative Summary STAT3 prevents v-src mediated cellular transformation (Bromberg et al. , 1998). Taken together with the obser-The JAK/STAT signaling pathway, renowned for its vation that STAT3 is frequently constitutively activated effects on cell proliferation and survival, is constituin cancer cells, it is likely that STAT3 plays a role in tively active in various human cancers, including ovartumorigenesis and/or cancer progression. ian. We have found that JAK and STAT are required Most tumors derive from cells of epithelial origin; in to convert the border cells in the Drosophila ovary order to become metastatic, and thereby a serious from stationary, epithelial cells to migratory, invasive threat to human health, these cells must detach from cells. The ligand for this pathway, Unpaired (UPD), is the epithelium of origin and invade surrounding tissues, expressed by two central cells within the migratory ultimately reaching the bloodstream. This step in cancer cell cluster. Mutations in upd or jak cause defects