ArticleeLife2015
The transcriptional response to tumorigenic polarity loss in Drosophila.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
75 citing papers in PubMed, 125 citations in OpenAlex.
- Myc and Tor drive growth and cell competition in the regeneration blastema of Drosophila wing imaginal discs.Development (Cambridge, England) · 2025Article
- Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.Cancer letters · 2025Article
- EyaHOST, a modular genetic system for investigation of intercellular and tumor-host interactions in Drosophila melanogaster.Cell reports methods · 2025Article
- Interplay of EGFR, JNK, and ROS signaling in soma-germline communication in the Drosophila testis.Stem cell reports · 2025Article
- Myc and Tor drive growth and cell competition in the regeneration blastema ofbioRxiv : the preprint server for biology · 2025Article
- Epithelial cell-fate switch triggering ectopic ligand-receptor-mediated JAK-STAT signaling promotes tumorigenesis iniScience · 2025Article
- Epigenetic Regulation in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- Paraneoplastic renal dysfunction in fly cancer models driven by inflammatory activation of stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Local Ecdysone synthesis in a wounded epithelium sustains developmental delay and promotes regeneration in Drosophila.Development (Cambridge, England) · 2024Article
- Article
- Paraneoplastic renal dysfunction in fly cancer models driven by inflammatory activation of stem cells.bioRxiv : the preprint server for biology · 2024Article
- Local ecdysone synthesis in a wounded epithelium sustains developmental delay and promotes regeneration inbioRxiv : the preprint server for biology · 2024Article
- The Drosophila tumour suppressor Lgl and Vap33 activate the Hippo pathway through a dual mechanism.Journal of cell science · 2024Article
- Cell polarity changes in cancer initiation and progression.The Journal of cell biology · 2024Review
- Polycomb safeguards imaginal disc specification through control of the Vestigial-Scalloped complex.Development (Cambridge, England) · 2023Article
- Mutual repression between JNK/AP-1 and JAK/STAT stratifies senescent and proliferative cell behaviors during tissue regeneration.PLoS biology · 2023Article
- Polycomb safeguards imaginal disc specification through control of the Vestigial-Scalloped complex.bioRxiv : the preprint server for biology · 2023Article
- A Drosophila chemical screen reveals synergistic effect of MEK and DGKα inhibition in Ras-driven cancer.Disease models & mechanisms · 2023Article
- Distinct signaling signatures drive compensatory proliferation via S-phase acceleration.PLoS genetics · 2022Article
- Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Loss of polarity correlates with progression of epithelial cancers, but how plasma membrane misorganization drives oncogenic transcriptional events remains unclear. The polarity regulators of the Drosophila Scribble (Scrib) module are potent tumor suppressors and provide a model for mechanistic investigation. RNA profiling of Scrib mutant tumors reveals multiple signatures of neoplasia, including altered metabolism and dedifferentiation. Prominent among these is upregulation of cytokine-like Unpaired (Upd) ligands, which drive tumor overgrowth. We identified a polarity-responsive enhancer in upd3, which is activated in a coincident manner by both JNK-dependent Fos and aPKC-mediated Yki transcription. This enhancer, and Scrib mutant overgrowth in general, are also sensitive to activity of the Polycomb Group (PcG), suggesting that PcG attenuation upon polarity loss potentiates select targets for activation by JNK and Yki. Our results link epithelial organization to signaling and epigenetic regulators that control tissue repair programs, and provide insight into why epithelial polarity is tumor-suppressive.
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What OpenQuestion holds
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.