ArticlePLoS genetics2010
dMyc functions downstream of Yorkie to promote the supercompetitive behavior of hippo pathway mutant cells.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
107 citing papers in PubMed, 182 citations in OpenAlex.
- Cell competition driven by secreted ligands: Modeling liver metastasis of colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- The Hippo tumor suppressor pathway triggers non-cell autonomous tumorigenesis in Drosophila.EMBO reports · 2026Article
- From fitness to fate: Hippo-YAP-mediated cell competition influence on stem cells activity.Bioscience reports · 2026Review
- Tumour-host interactions in Drosophila: mechanisms in the tumour micro- and macroenvironment.Molecular oncology · 2026Review
- Combined MYC Activation and PTEN Loss Drives Molecular Features of Aggressive Preinvasive Lesions in Mouse Prostate.Molecular cancer research : MCR · 2026Article
- EyaHOST, a modular genetic system for investigation of intercellular and tumor-host interactions in Drosophila melanogaster.Cell reports methods · 2025Article
- Mechanisms of cellular fitness and cell competition: Towards an integrated view.Current opinion in cell biology · 2025Review
- Neural cell competition sculpting brain from cradle to grave.National science review · 2025Review
- Nonautonomous Regulation of Tumor Growth.Advances in experimental medicine and biology · 2025Review
- Unveiling the Tumor Suppressors: Insights from Drosophila.Advances in experimental medicine and biology · 2025Review
- Article
- An expanded view of cell competition.Development (Cambridge, England) · 2024Review
- Mechanisms of Germline Stem Cell Competition across Species.Life (Basel, Switzerland) · 2024Review
- Ribosome stalling duringPNAS nexus · 2024Article
- YAP, TAZ, and Hippo-Dysregulating Fusion Proteins in Cancer.Annual review of cancer biology · 2024Article
- Article
- Young glial progenitor cells competitively replace aged and diseased human glia in the adult chimeric mouse brain.Nature biotechnology · 2024Article
- Peritoneal Microenvironment Promotes Appendiceal Adenocarcinoma Growth: A Multi-omics Approach Using Patient-Derived Xenografts.Molecular cancer research : MCR · 2024Article
- Review
47 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
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Genetic analyses in Drosophila epithelia have suggested that the phenomenon of "cell competition" could participate in organ homeostasis. It has been speculated that competition between different cell populations within a growing organ might play a role as either tumor promoter or tumor suppressor, depending on the cellular context. The evolutionarily conserved Hippo (Hpo) signaling pathway regulates organ size and prevents hyperplastic disease from flies to humans by restricting the activity of the transcriptional cofactor Yorkie (yki). Recent data indicate also that mutations in several Hpo pathway members provide cells with a competitive advantage by unknown mechanisms. Here we provide insight into the mechanism by which the Hpo pathway is linked to cell competition, by identifying dMyc as a target gene of the Hpo pathway, transcriptionally upregulated by the activity of Yki with different binding partners. We show that the cell-autonomous upregulation of dMyc is required for the supercompetitive behavior of Yki-expressing cells and Hpo pathway mutant cells, whereas the relative levels of dMyc between Hpo pathway mutant cells and wild-type neighboring cells are critical for determining whether cell competition promotes a tumor-suppressing or tumor-inducing behavior. All together, these data provide a paradigmatic example of cooperation between tumor suppressor genes and oncogenes in tumorigenesis and suggest a dual role for cell competition during tumor progression depending on the output of the genetic interactions occurring between confronted cells.
Indexed as
Identifiers
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.