ReviewDevelopment, growth & differentiation2019
Elimination of oncogenic cells that regulate epithelial homeostasis in Drosophila.
Review in Development, growth & differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Elevation of major constitutive heat shock proteins is heat shock factor independent and essential for establishment and growth of Lgl loss and Yorkie gain-mediated tumors in Drosophila.Cell stress & chaperones · 2022Article
- Rounding up the Usual Suspects: Assessing Yorkie, AP-1, and Stat Coactivation in Tumorigenesis.International journal of molecular sciences · 2020Article
- Two-Faced: Roles of JNK Signalling During Tumourigenesis in theFrontiers in cell and developmental biology · 2020Review
- Elimination of oncogenic cells that regulate epithelial homeostasis in Drosophila.Development, growth & differentiation · 2019Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Normal epithelial tissues often put anti-tumorigenic pressure on newly emerged oncogenic cells through cell-cell communications. In Drosophila epithelium, clones of oncogenic cells mutant for evolutionarily conserved apico-basal polarity genes such as scribble (scrib) and discs large (dlg) are actively eliminated when surrounded by normal cells. It has been reported that c-Jun N-terminal kinase (JNK) signaling in polarity-deficient cells is crucial for their cell death. However, the mechanism by which normal epithelial tissues exert anti-tumorigenic effects on polarity-deficient cells had been elusive. Here, I describe our genetic studies in Drosophila epithelium especially focused on the role of surrounding normal epithelial cells in response to the emergence of polarity-deficient cells. Furthermore, I also describe recent studies regarding the mechanism by which polarity-deficient cells are extruded from the tissue, and discuss future perspectives on the study of cell-cell communications in epithelial homeostasis.
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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.