Expression data from MAP3K11/GDF15 axis is a critical driver of cancer cachexia

MAP3K11 overexpression in tumors leads to weight loss in the host We assessed the ability of potential tumor maintenance genes to drive tumor growth in vivo using a directed complementation (DC) approach. This assay involves testing the ability of an introduced gene to maintain tumor growth when expression of an inducible driving oncogene is turned off. In this case, we tested the ability of MAP3K7/TAK1 or MAP3K11/MLK3 to form tumors in vivo in a genetically engineered model originally driven by a doxycycline-inducible HER2(V659E) oncogene. In this system, the expression and activity of HER2 was suppressed by doxycycline withdrawal and followed by the introduction of one of 13 genes (ErbB3, FAK1, FGFR2aIIIb, FGFR2aIIIc, FGFR3, HER2, MAP3K11, PIP5K1B, RONd160, RON+MSP, RSK2, MAP3K7, TNK2)