ArticleOncogene2014
Drosophila actin-Capping Protein limits JNK activation by the Src proto-oncogene.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Proteome Unravels Mechanism Differences in Embryogenesis Between Honey Bee Drone and Worker (Apis mellifera L.).Molecular & cellular proteomics : MCP · 2026Article
- Control of mitochondrial dynamics by the metabolic regulator dPGC1 limits Yorkie-induced oncogenic growth in Drosophila.PLoS biology · 2025Article
- Turn-on protein switches for controlling actin binding in cells.Nature communications · 2024Article
- Turn-On Protein Switches for Controlling Actin Binding in Cells.bioRxiv : the preprint server for biology · 2023Article
- Activation of an actin signaling pathway in pre-malignant mammary epithelial cells by P-cadherin is essential for transformation.Disease models & mechanisms · 2023Article
- WASH activation controls endosomal recycling and EGFR and Hippo signaling during tumor-suppressive cell competition.Nature communications · 2022Article
- Methionine restriction breaks obligatory coupling of cell proliferation and death by an oncogene Src ineLife · 2021Article
- MKK3 modulates JNK-dependent cell migration and invasion.Cell death & disease · 2019Article
- Article
- Mechanical strain regulates the Hippo pathway inDevelopment (Cambridge, England) · 2018Article
- Hippo, TGF-β, and Src-MAPK pathways regulate transcription of the upd3 cytokine in Drosophila enterocytes upon bacterial infection.PLoS genetics · 2017Article
- MRL proteins cooperate with activated Ras in glia to drive distinct oncogenic outcomes.Oncogene · 2017Article
- Actin stress fiber organization promotes cell stiffening and proliferation of pre-invasive breast cancer cells.Nature communications · 2017Article
- Regulation of Hippo signalling by p38 signalling.Journal of molecular cell biology · 2016Article
- YAP and TAZ in epithelial stem cells: A sensor for cell polarity, mechanical forces and tissue damage.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016Review
- Integrin signalling regulates YAP and TAZ to control skin homeostasis.Development (Cambridge, England) · 2016Article
- Rho1-Wnd signaling regulates loss-of-cell polarity-induced cell invasion in Drosophila.Oncogene · 2016Article
- The Notch-mediated hyperplasia circuitry in Drosophila reveals a Src-JNK signaling axis.eLife · 2015Article
- Cooperation of the BTB-Zinc finger protein, Abrupt, with cytoskeletal regulators in Drosophila epithelial tumorigenesis.Biology open · 2015Article
- Src kinase function controls progenitor cell pools during regeneration and tumor onset in the Drosophila intestine.Oncogene · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Src family kinases c-Src, and its downstream effectors, the Rho family of small GTPases RhoA and Jun N-terminal kinase (JNK) have a significant role in tumorigenesis. In this report, using the Drosophila wing disc epithelium as a model system, we demonstrate that the actin-Capping Protein (CP) αβ heterodimer, which regulates actin filament (F-actin) polymerization, limits Src-induced apoptosis or tissue overgrowth by restricting JNK activation. We show that overexpressing Src64B drives JNK-independent loss of epithelial integrity and JNK-dependent apoptosis via Btk29A, p120ctn and Rho1. However, when cells are kept alive with the Caspase inhibitor P35, JNK acts as a potent inducer of proliferation via activation of the Yorkie oncogene. Reducing CP levels direct apoptosis of overgrowing Src64B-overexpressing tissues. Conversely, overexpressing capping protein inhibits Src64B and Rho1, but not Rac1-induced JNK signaling. CP requires the actin-binding domain of the α-subunit to limit Src64B-induced apoptosis, arguing that the control of F-actin mediates this effect. In turn, JNK directs F-actin accumulation. Moreover, overexpressing capping protein also prevents apoptosis induced by ectopic JNK expression. Our data are consistent with a model in which the control of F-actin by CP limits Src-induced apoptosis or tissue overgrowth by acting downstream of Btk29A, p120ctn and Rho1, but upstream of JNK. In turn, JNK may counteract the effect of CP on F-actin, providing a positive feedback, which amplifies JNK activation. We propose that cytoskeletal changes triggered by misregulation of F-actin modulators may have a significant role in Src-mediated malignant phenotypes during the early stages of cellular transformation.
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