Cell-cell signaling interactions are of immense significance to both normal, and tumor cells. Alterations in these signaling interactions cause critical changes in cell behavior, and may underlie diseases like cancer where cells are capable of unrestrained proliferation. Studies in Drosophila imaginal discs have identified key cell-cell interactions like cell competition, and key molecular signals (Wingless, Dronc, Jun N-terminal Kinase, Yorkie) that regulate these intercellular interactions. These signals also play important roles during compensatory proliferation- a response that cells employ to restore tissue homeostasis. However, if these intercellular interactions are involved in the aggressive growth of cancers remains poorly understood. Using the well-established in-vivo clonal models in flies, we found that RasV12, scrib- cells behave like ‘supercompetitor winner cells’. Furthermore, Wg, Dronc, JNK, and Yki are all upregulated in RasV12, scrib- cells, and downregulation of these signals leads to reduction in tumor growth suggesting that these signals are required for the growth of RasV12, scrib- tumors. We identified that Yki, and JNK activities are simultaneously induced in RasV12, scrib- cells, and JNK-Yki form a self-reinforcing positive feedback loop downstream of Wg and Dronc that plays a key role in promoting tumorigenesis in RasV12, scrib- cells. The signal amplification loop is important for aggressive tumor growth, as activation of this loop does not occur in instances where oncogenes are individually activated or when apical-basal polarity is lost. We have thus identified a novel molecular network in which Wg dependent activation of Dronc controls a JNK-Yki mediated positive feedback signal amplification loop that promotes tumor growth. Our findings are important because tumor cell specific molecular networks may generate key insights into signaling interactions during oncogenic cooperation, and therefore provide a powerful model for reconstructing key biologically meaningful changes in signaling pathways that drive growth, and altered signaling in cancer cells in flies and humans.