ArticleCancer research2007
Differing Src signaling levels have distinct outcomes in Drosophila.
Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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
42 citing papers in PubMed, 60 citations in OpenAlex.
- Chemical programming of kinase inhibitors in a modular chemputer-based system.Communications biology · 2026Article
- Tumour-host interactions in Drosophila: mechanisms in the tumour micro- and macroenvironment.Molecular oncology · 2026Review
- An exploratory analysis of the effects of human FYN and its Drosophila ortholog in Drosophila tissues.Scientific reports · 2026Article
- Activation of a Src-JNK pathway in unscheduled endocycling cells of the Drosophila wing disc induces a chronic wounding response.Genetics · 2025Article
- Using Drosophila to uncover the role of organismal physiology and the tumor microenvironment in cancer.Trends in cancer · 2024Review
- Concurrent targeting of GSK3 and MEK as a therapeutic strategy to treat pancreatic ductal adenocarcinoma.Cancer science · 2024Article
- An allosteric switch between the activation loop and a c-terminal palindromic phospho-motif controls c-Src function.Nature communications · 2023Article
- Apoptosis inhibition restrains primary malignant traits in differentFrontiers in cell and developmental biology · 2022Article
- Article
- A Drosophila platform identifies a novel, personalized therapy for a patient with adenoid cystic carcinoma.iScience · 2021Article
- Integrated computational and Drosophila cancer model platform captures previously unappreciated chemicals perturbing a kinase network.PLoS computational biology · 2019Article
- MKK3 modulates JNK-dependent cell migration and invasion.Cell death & disease · 2019Article
- Article
- Non-mammalian models of multiple endocrine neoplasia type 2.Endocrine-related cancer · 2018Review
- Modelling Cooperative Tumorigenesis inBioMed research international · 2018Review
- Drosophila as a Model to Study the Link between Metabolism and Cancer.Journal of developmental biology · 2017Review
- 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
- Invadosomes in their natural habitat.European journal of cell biology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
High levels of Src activity are found in a broad spectrum of cancers. The roles of Src and its negative regulator Csk have been extensively studied, although results have often proved contradictory or the relevance to whole organisms is unclear. In Drosophila, overexpression of either Src orthologue resulted in apoptotic cell death, but paradoxically, reducing dCsk activity led to over-proliferation and tissue overgrowth. Here, we show that in Drosophila epithelia in situ, the levels of Src signaling determine the cellular outcome of Src activation. Apoptotic cell death was triggered specifically at high Src signaling levels; lower levels directed antiapoptotic signals while promoting proliferation. Furthermore, our data indicate that expression of kinase-dead Src isoforms do not necessarily act as dominant-negative factors, but can instead increase Src pathway activity, most likely by titrating Csk activity away from endogenous Src. The importance of Src activity levels was emphasized when we examined oncogenic cooperation between Src and Ras: malignant overgrowth was observed specifically when high Src signaling levels were achieved. We propose a model in which low levels of Src signaling promote survival and proliferation during early stages of tumorigenesis, whereas strong Src signaling, coupled with antiapoptotic signals, directs invasive migration and metastasis during advanced tumor stages.
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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.