ArticleDevelopmental cell2016
Slit-Robo Repulsive Signaling Extrudes Tumorigenic Cells from Epithelia.
Article in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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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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
47 citing papers in PubMed, 82 citations in OpenAlex.
- Unveiling the Tumor Suppressors: Insights from Drosophila.Advances in experimental medicine and biology · 2025Review
- Using Drosophila to uncover the role of organismal physiology and the tumor microenvironment in cancer.Trends in cancer · 2024Review
- Cell competition for neuron-derived trophic factor controls the turnover and lifespan of microglia.Science advances · 2023Article
- Homophilic interaction of cell adhesion molecule 3 coordinates retina neuroepithelial cell proliferation.The Journal of cell biology · 2023Article
- Epidermal growth factor receptor signaling protects epithelia from morphogenetic instability and tissue damage in Drosophila.Development (Cambridge, England) · 2023Article
- Review
- The CRL4 E3 ligase Mahjong/DCAF1 controls cell competition through the transcription factor Xrp1, independently of polarity genes.Development (Cambridge, England) · 2022Article
- Cell adhesion molecule BVES functions as a suppressor of tumor cells extrusion in hepatocellular carcinoma metastasis.Cell communication and signaling : CCS · 2022Article
- Game of clones: Battles in the field of carcinogenesis.Pharmacology & therapeutics · 2022Review
- Hepatocyte growth factor derived from senescent cells attenuates cell competition-induced apical elimination of oncogenic cells.Nature communications · 2022Article
- Early construction of the thalamocortical axon pathway requires c-Jun N-terminal kinase signaling within the ventral forebrain.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Article
- Forced into shape: Mechanical forces in Drosophila development and homeostasis.Seminars in cell & developmental biology · 2021Review
- EPHA2-dependent outcompetition of KRASG12D mutant cells by wild-type neighbors in the adult pancreas.Current biology : CB · 2021Article
- Early loss of Scribble affects cortical development, interhemispheric connectivity and psychomotor activity.Scientific reports · 2021Article
- The neurorepellent, Slit2, prevents macrophage lipid loading by inhibiting CD36-dependent binding and internalization of oxidized low-density lipoprotein.Scientific reports · 2021Article
- Slit/Robo Signaling Regulates Multiple Stages of the Development of theFrontiers in cell and developmental biology · 2021Article
- Emerging mechanisms of cell competition.Nature reviews. Genetics · 2020Review
- Stem Cell DNA Damage and Genome Mutation in the Context of Aging and Cancer Initiation.Cold Spring Harbor perspectives in biology · 2020Review
- Mechanism of tumor-suppressive cell competition in flies.Cancer science · 2020Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cells dynamically interact throughout animal development to coordinate growth and deter disease. For example, cell-cell competition weeds out aberrant cells to enforce homeostasis. In Drosophila, tumorigenic cells mutant for the cell polarity gene scribble (scrib) are actively eliminated from epithelia when surrounded by wild-type cells. While scrib cell elimination depends critically on JNK signaling, JNK-dependent cell death cannot sufficiently explain scrib cell extirpation. Thus, how JNK executed cell elimination remained elusive. Here, we show that repulsive Slit-Robo2-Ena signaling exerts an extrusive force downstream of JNK to eliminate scrib cells from epithelia by disrupting E-cadherin. While loss of Slit-Robo2-Ena in scrib cells potentiates scrib tumor formation within the epithelium, Robo2-Ena hyperactivation surprisingly triggers luminal scrib tumor growth following excess extrusion. This extrusive signaling is amplified by a positive feedback loop between Slit-Robo2-Ena and JNK. Our observations provide a potential causal mechanism for Slit-Robo dysregulation in numerous human cancers.
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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.