ArticleOncogene2001
Studies on human colon cancer gene APC by targeted expression in Drosophila.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Fruit fly for anticancer drug discovery and repurposing.Annals of medicine and surgery (2012) · 2023Article
- Overview of research progress and application of experimental models of colorectal cancer.Frontiers in pharmacology · 2023Review
- Article
- A Personalized Therapeutics Approach Using anFrontiers in oncology · 2021Article
- A Drosophila Based Cancer Drug Discovery Framework.Advances in experimental medicine and biology · 2019Review
- Anti-cancer drug discovery: update and comparisons in yeast, Drosophila, and zebrafish.Current molecular pharmacology · 2014Article
- Drosophila-based in vivo assay for the validation of inhibitors of the epidermal growth factor receptor/Ras pathway.Journal of biosciences · 2008Article
- Human APC sequesters beta-catenin even in the absence of GSK-3beta in a Drosophila model.Oncogene · 2008Article
- Genetic identification of effectors downstream of Neu (ErbB-2) autophosphorylation sites in a Drosophila model.Oncogene · 2003Article
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Authors and funding
2 authors.
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Abstract
Mutations in human Adenomatous Polyposis Coli (APC) gene are associated with both familial and sporadic colorectal tumors. APC is known to down regulate beta-catenin levels, a transducer of Wnt signaling. The aim of this study is to provide transgenic Drosophila expressing either full-length or truncated forms of human APC (hAPC) protein and methods for using them in functional genomics and drug screening. Consistent with its biochemical properties, targeted expression of either full-length hAPC or its beta-catenin binding domain alone negatively regulated the function of the beta-catenin homologue, Armadillo (Arm) and thereby, inhibited Wnt/Wg signaling during fly development. hAPC inhibited Arm function even in the absence of GSK-3beta activity, although the latter was required to mediate the degradation of Arm. Consistent with this, hAPC suppressed the phenotypes induced by the over-expression of degradation-resistant forms of Arm. Subsequently, using hAPC-induced eye phenotypes as the assay in a suppressor-enhancer screen, we have identified two new loci in Drosophila, which modulate Wnt/Wg signaling. In addition, an anti-colon cancer drug, indomethacin, specifically enhanced hAPC-induced phenotypes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.