Arushi Rai


Presentation: 10:45-12:00, Kennedy Union Ballroom



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Studies with Drosophila RasV12,scrib-/- tumor models have shown that Yorkie, the effector molecule of the Hippo pathway, interacts with other signaling pathways to form a dynamic transcriptional network within cancer cells. Previously, we have shown that in RasV12,scrib-/- cells Wingless (Wg) acts upstream of Caspases, JNK, and Yki forming a tumor-specific network that regulates tumor growth and development. By studying this complex network, we aim to unravel the key players that regulate tumor growth. Wg appears upstream of the molecular network and is also a transcriptional target of Yorkie. Wg expression is ectopically induced in RasV12 and RasV12,scrib-/- tumor clones. However, accumulation of Wg is reduced in tumor clones with heterozygous loss of yki (ykiB5/+;RasV12,scrib-/-) or downregulation of Wg signaling (dTCFDN; RasV12,scrib-/-). Heterozygosity of yki (ykiB5/+;RasV12,scrib-/-) and downregulation of Wg signaling (dTCFDN; RasV12,scrib-/-) both resulted in reduced tumor clone size in comparison to RasV12,scrib-/- tumor clones. To further understand the molecular mechanism by which Wg and Yki promote tumor growth, we will investigate the effect of downregulation of Wg pathway and Hippo pathway on the (a) the transcriptional network of RasV12,scrib-/- tumor clones by analyzing the mRNA expression by qRT-PCR and (b) hallmarks of cancer such as invasion, cell adhesion, and survival signaling by immunohistochemistry-based approach (c) analyzing the Hippo pathway (Mst,p-MST), JNK pathway (JNK,p-JNK) and Wg pathway activity by Western blot assay. Here, we present our progress on the organization of the molecular network that involves Wingless and Yorkie.

Publication Date


Project Designation

Graduate Research

Primary Advisor

Madhuri Kango-Singh, Amit Singh

Primary Advisor's Department



Stander Symposium, College of Arts and Sciences

Modulation of Tumor Growth by Yorkie and Wingless