ArticleNature genetics2009
A tumor suppressor activity of Drosophila Polycomb genes mediated by JAK-STAT signaling.
Article in Nature genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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
92 citing papers in PubMed.
- More than SAM: mechanisms of action of the Polycomb group protein polyhomeotic.Nucleus (Austin, Tex.) · 2026Review
- Psc and Su(z)2 safeguard intestinal stem cell identity and prevent chinmo-dependent tumorigenesis.EMBO reports · 2026Article
- A tumor-suppressive role of the PRC1 Polycomb epigenetic complex in the maintenance of adult Drosophila intestinal stem cell identity.PLoS genetics · 2026Article
- Article
- Toll receptors mediate tissue intrinsic surveillance against aberrant cells by detecting cell fate aberrations.Development (Cambridge, England) · 2026Article
- Myc and Tor drive growth and cell competition in the regeneration blastema of Drosophila wing imaginal discs.Development (Cambridge, England) · 2025Article
- Myc and Tor drive growth and cell competition in the regeneration blastema ofbioRxiv : the preprint server for biology · 2025Article
- A disordered linker in the Polycomb protein Polyhomeotic tunes phase separation and oligomerization.Molecular cell · 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
- Hyd/UBR5 defines a tumor suppressor pathway that links Polycomb repressive complex to regulated protein degradation in tissue growth control and tumorigenesis.Genes & development · 2024Article
- Sustained inactivation of the Polycomb PRC1 complex induces DNA repair defects and genomic instability in epigenetic tumors.Histochemistry and cell biology · 2024Article
- Article
- Sustained inactivation of the Polycomb PRC1 complex induces DNA repair defects and genomic instability in epigenetic tumors.Research square · 2024Article
- A Two-Step Mechanism for Creating Stable, Condensed Chromatin with the Polycomb Complex PRC1.Molecules (Basel, Switzerland) · 2024Article
- Regenerative growth is constrained by brain tumor to ensure proper patterning in Drosophila.PLoS genetics · 2023Article
- 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
- Bilateral JNK activation is a hallmark of interface surveillance and promotes elimination of aberrant cells.eLife · 2023Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
A prevailing paradigm posits that Polycomb Group (PcG) proteins maintain stem cell identity by repressing differentiation genes, and abundant evidence points to an oncogenic role for PcG proteins in human cancer. Here we show using Drosophila melanogaster that a conventional PcG complex can also have a potent tumor suppressor activity. Mutations in any core PRC1 component cause pronounced hyperproliferation of eye imaginal tissue, accompanied by deregulation of epithelial architecture. The mitogenic JAK-STAT pathway is strongly and specifically activated in mutant tissue; activation is driven by transcriptional upregulation of Unpaired (Upd, also known as Outstretched, Os) family ligands. We show here that upd genes are direct targets of PcG-mediated repression in imaginal discs. Ectopic JAK-STAT activity is sufficient to induce overproliferation, whereas reduction of JAK-STAT activity suppresses the PRC1 mutant tumor phenotype. These findings show that PcG proteins can restrict growth directly by silencing mitogenic signaling pathways, shedding light on an epigenetic mechanism underlying tumor suppression.
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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.