ArticleNature2017
The ligand Sas and its receptor PTP10D drive tumour-suppressive cell competition.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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
81 citing papers in PubMed, 158 citations in OpenAlex.
- Filamin-ETV4/5 acts as mechanosensor-mechanotransducer axis that drives cell competition-mediated elimination of transformed cells.Nature communications · 2026Article
- Hbs and Rst adhesion molecules provide a regional code that regulates cell elimination during epithelial remodeling.iScience · 2026Article
- From fitness to fate: Hippo-YAP-mediated cell competition influence on stem cells activity.Bioscience reports · 2026Review
- Winners take it all: turning cell competition into a therapeutic ally.Cell communication and signaling : CCS · 2026Review
- Article
- Imaging Cell Competition in Ex-VivoMethods and protocols · 2025Article
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- Physical traits of supercompetitors in cell competition.Journal of the Royal Society, Interface · 2025Article
- RhoGEF2 overexpression induces cell competition dependent on Ptp10D, Crumbs and the Hippo signaling pathway.Journal of cell science · 2025Article
- The cell-adhesion molecule Echinoid promotes tissue survival and separately restricts tissue overgrowth.Development (Cambridge, England) · 2025Article
- Adipose tissue-secreted Spz5 promotes distal tumor progression via Toll-6-mediated Hh pathway activation in Drosophila.The EMBO journal · 2025Article
- Repulsive interactions instruct synaptic partner matching in an olfactory circuit.bioRxiv : the preprint server for biology · 2025Article
- Spatial and temporal signatures of cell competition revealed by K-function analysis.Molecular biology of the cell · 2025Article
- Epithelial cell-fate switch triggering ectopic ligand-receptor-mediated JAK-STAT signaling promotes tumorigenesis iniScience · 2025Article
- Repulsive interactions instruct synaptic partner matching in an olfactory circuit.Research square · 2025Article
- Unveiling the Tumor Suppressors: Insights from Drosophila.Advances in experimental medicine and biology · 2025Review
- Article
- Cell competition and cancer from Drosophila to mammals.Oncogenesis · 2024Review
- Cell competition for neuron-derived trophic factor controls the turnover and lifespan of microglia.Science advances · 2023Article
- Zebrafish imaging reveals hidden oncogenic-normal cell communication during primary tumorigenesis.Cell structure and function · 2023Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normal epithelial cells often exert anti-tumour effects against nearby oncogenic cells. In the Drosophila imaginal epithelium, clones of oncogenic cells with loss-of-function mutations in the apico-basal polarity genes scribble or discs large are actively eliminated by cell competition when surrounded by wild-type cells. Although c-Jun N-terminal kinase (JNK) signalling plays a crucial role in this cell elimination, the initial event, which occurs at the interface between normal cells and polarity-deficient cells, has not previously been identified. Here, through a genetic screen in Drosophila, we identify the ligand Sas and the receptor-type tyrosine phosphatase PTP10D as the cell-surface ligand-receptor system that drives tumour-suppressive cell competition. At the interface between the wild-type 'winner' and the polarity-deficient 'loser' clones, winner cells relocalize Sas to the lateral cell surface, whereas loser cells relocalize PTP10D there. This leads to the trans-activation of Sas-PTP10D signalling in loser cells, which restrains EGFR signalling and thereby enables elevated JNK signalling in loser cells, triggering cell elimination. In the absence of Sas-PTP10D, elevated EGFR signalling in loser cells switches the role of JNK from pro-apoptotic to pro-proliferative by inactivating the Hippo pathway, thereby driving the overgrowth of polarity-deficient cells. These findings uncover the mechanism by which normal epithelial cells recognize oncogenic polarity-deficient neighbours to drive cell competition.
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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 Socratic graph.