FIGURE 3.

Pro-tumourigenic JNK signalling. JNK signalling in the face of apoptosis-suppressing signals, like that which occur via Ras-MAPK signalling in Ras85D^V12/scrib^–/– tumours, is co-opted to promote several tumourigenic behaviours. JNK signalling in these tumours is activated via some combination of Egr-mediated TNFR activation and Rho1-Wnd signalling – the proportions of each are not fully understood, but TNF signalling has been shown to be dispensable. JNK signalling suppresses differentiation in Ras85D^V12/scrib^–/– tumours, but the precise mechanism of this interaction is unclear. JNK signalling also appears to suppress SWH signalling, allowing Yki to promote the survival and overproliferation of the tumourous cells. Jak-STAT signalling, initiated by the Upd-family ligands whose expression is promoted by JNK signalling, also contributes to tumourigenic survival and overproliferation. Lastly, JNK signalling promotes invasiveness of the tumour cells and basement membrane degradation by upregulating proteins such as Mmp1. Gene and protein name abbreviations used in the diagram are as follows: Eiger (Egr), Grindelwald (Grnd), Wengen (Wgn), Wallenda (Wnd), unpaired 1 (upd1), unpaired 2 (upd2), unpaired 3 (upd3), Matrix metalloproteinase 1 (Mmp1), Yorkie (Yki), Cyclin E (CycE), Death-associated inhibitor of apoptosis 1 (Diap1), reaper (rpr), head involution defective (hid).