Cancer is a multi-faceted disease that can affect all tissue compartments, resulting in a spectrum of subtypes. Despite extensive research, cancers originating in epithelial tissues – termed epithelial cancers or carcinomas, remain largely represented in cancer diagnosis and mortality. Indeed, a number of cancer hallmarks have been established including loss of apical-basal (AB) cell polarity in carcinomas. Previously, our lab conducted an RNAi based mammalian genetic screen and identified Nance-Horan Syndrome (NHS) as a key player in Scribble (SCRIB)- mediated RASV12 suppression. Here, Drosophila melanogaster was used to investigate Guk-Holder (GukH), the Drosophila orthologue of NHS, as a potential regulator of Scribble-mediated epithelial AB polarity. Immunofluorescent staining indicated co-localization between GukH, Scrib and Dlg (Discs-Large) in epithelial tissues, however GukH does not appear to regulate their localization, nor does its loss replicate or enhance the migratory phenotype of scrib or dlg loss. These experiments suggests that GukH may have Scribble module-independent functions in Drosophila. Interestingly, analysis examining the expression of gukh in vivo whilst altering signalling pathways identified the Decapentaplegic (TGF-β in mammals) and Ras-MAPK pathways as novel regulators of gukh expression. Consistent with these findings was the identification of putative transcription factor binding sites for downstream regulators of these pathways in the promoter region of gukh, and slight suppression of Ras activation-induced eye growth by gukh mutants. Furthermore, mutant gukh MARCM clones demonstrated a slight competitive advantage. Using mitotic recombinant clones, gukh loss decreased cell proliferation and cell death cell- and non-cell autonomously. Overall, GukH does not appear to play a role in AB polarity, however I have shown novel involvement in cell proliferation and apoptosis regulation, linking its function to pathways critical in development and cancer progression. Future work entails confirmation of these links and understanding whether the molecular and cellular properties of GukH are conserved in mammalian cancer.