ArticleNature communications2018
Short-term activation of the Jun N-terminal kinase pathway in apoptosis-deficient cells of Drosophila induces tumorigenesis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed, 65 citations in OpenAlex.
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- Tumour-host interactions in Drosophila: mechanisms in the tumour micro- and macroenvironment.Molecular oncology · 2026Review
- The homeodomain-interacting protein kinase Hipk promotes apoptosis by stabilizing the active form of Dronc.Cell death discovery · 2025Article
- A threshold level of JNK activates damage-responsive enhancers via JAK/STAT to promote tissue regeneration.Development (Cambridge, England) · 2025Article
- Pyruvate kinase deficiency links metabolic perturbations to neurodegeneration and axonal protection.Molecular metabolism · 2025Article
- Replication stress promotes cellular transformation in Drosophila epithelium.Cell death discovery · 2025Article
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- Regeneration following tissue necrosis is mediated by non-apoptotic caspase activity.bioRxiv : the preprint server for biology · 2024Article
- Compressive stresses in cancer: characterization and implications for tumour progression and treatment.Nature reviews. Cancer · 2024Review
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- Lack of apoptosis leads to cellular senescence and tumorigenesis in Drosophila epithelial cells.Cell death discovery · 2023Article
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- Mutual repression between JNK/AP-1 and JAK/STAT stratifies senescent and proliferative cell behaviors during tissue regeneration.PLoS biology · 2023Article
- Gbb Regulates Blood Cell Proliferation and Differentiation through JNK and EGFR Signaling Pathways in theCells · 2023Article
- Size compensation inFrontiers in cell and developmental biology · 2023Article
- Imaginal Disc Regeneration: Something Old, Something New.Cold Spring Harbor perspectives in biology · 2022Review
- Non-apoptotic activation of Drosophila caspase-2/9 modulates JNK signaling, the tumor microenvironment, and growth of wound-like tumors.Cell reports · 2022Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Drosophila, the JNK pathway eliminates by apoptosis aberrant cells that appear in development. It also performs other functions associated with cell proliferation, but analysis of the latter is hindered by the pro-apoptotic activity. We report the response of apoptosis-deficient cells to transient activation of JNK and show that it causes persistent JNK function during the rest of the development. As a consequence, there is continuous activity of the downstream pathways JAK/STAT, Wg and Dpp, which results in tumour overgrowths. We also show that the oncogenic potential of the Ras-MAPK pathway resides largely on its ability to suppress apoptosis. It has been proposed that a hallmark of tumour cells is that they can evade apoptosis. In reverse, we propose that, in Drosophila, apoptosis-deficient cells become tumorigenic due to their property of acquiring persistent JNK activity after stress events that are inconsequential in tissues in which cells are open to apoptosis.
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