ArticleDevelopmental cell2024
Senescent cells and macrophages cooperate through a multi-kinase signaling network to promote intestinal transformation in Drosophila.
Article in Developmental cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Macrophage restriction inScience advances · 2026Article
- Beyond Mice and Men: Alternative Vertebrate and Invertebrate Models in Cancer Biology.Annual review of cancer biology · 2026Article
- Applications and challenges of Drosophila melanogaster as a laboratory model in human cancer research: a narrative review.Discover oncology · 2025Review
- Multi-target synergistic anti-aging: QG extends Caenorhabditis elegans lifespan through DAF-16/FOXO pathways, mitochondrial homeostasis and metabolic reprogramming.Biogerontology · 2025Article
- Trends in intestinal aging: From underlying mechanisms to therapeutic strategies.Acta pharmaceutica Sinica. B · 2025Review
- Targeted nanoparticle delivery system for tumor-associated macrophage reprogramming to enhance TNBC therapy.Cell biology and toxicology · 2025Article
- Host-Microbe Interactions in Drosophila Cancer.Advances in experimental medicine and biology · 2025Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
Cellular senescence is a conserved biological process that plays a crucial and context-dependent role in cancer. The highly heterogeneous and dynamic nature of senescent cells and their small numbers in tissues make in vivo mechanistic studies of senescence challenging. As a result, how multiple senescence-inducing signals are integrated in vivo to drive senescence in only a small number of cells is unclear. Here, we identify cells that exhibit multiple features of senescence in a Drosophila model of intestinal transformation, which emerge in response to concurrent activation of AKT, JNK, and DNA damage signaling within transformed tissue. Eliminating senescent cells, genetically or by treatment with senolytic compounds, reduces overgrowth and improves survival. We find that senescent cells promote tumorigenesis by recruiting Drosophila macrophages to the transformed tissue, which results in non-autonomous activation of JNK signaling. These findings identify senescent cell-macrophage interactions as an important driver of epithelial transformation.
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Registered trials
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