Fig. 7.

A tripartite TF network drives tumor malignancy. A model summarizing unique and common roles of Fos, Ets21c and Ftz-F1 in tumor malignancy that is provoked by oncogenic Ras signaling and the loss of the apico-basal polarity gene scribble. Fos and Ftz-F1 are both required for tumor invasiveness. While Fos prevents differentiation, Ftz-F1 contributes to tumor growth, possibly by deregulating Hpo/Yki signaling. Ets21c serves to fine-tune tumor gene expression. The oncogenic activity of Fos depends on its phosphorylation by JNK. Ets21c and Ftz-F1 are regulated transcriptionally, and unknown inputs additional to JNK are likely to control their activity. While Ets21c promotes tumor growth in a JNK-independent manner, Ets21c can uniquely substitute for loss of polarity and stimulate invasiveness through a feedforward loop, hijacking JNK activity.