ArticleGenetics2011
Identification of novel Ras-cooperating oncogenes in Drosophila melanogaster: a RhoGEF/Rho-family/JNK pathway is a central driver of tumorigenesis.
Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 85 citations in OpenAlex.
- From Fly to Human: Translational Relevance ofInternational journal of molecular sciences · 2026Review
- Dysregulation of Glial Gap Junction Protein Innexin2 Mediates Seizures and Disrupted Sleep in a Drosophila Model for North Sea Progressive Myoclonus Epilepsy.Journal of neuroscience research · 2025Article
- RhoGEF2 overexpression induces cell competition dependent on Ptp10D, Crumbs and the Hippo signaling pathway.Journal of cell science · 2025Article
- A feed-forward loop between Toll/NF-κB and Rac1 promotes epithelial to mesenchymal transition of Ras-oncogenic hindgut enterocytes in Drosophila.Biology open · 2025Article
- Vitamin B6 deficiency cooperates with oncogenic Ras to induce malignant tumors in Drosophila.Cell death & disease · 2024Article
- Non-Mammalian Models for Understanding Neurological Defects in RASopathies.Biomedicines · 2024Review
- Using Drosophila to uncover the role of organismal physiology and the tumor microenvironment in cancer.Trends in cancer · 2024Review
- A Drosophila chemical screen reveals synergistic effect of MEK and DGKα inhibition in Ras-driven cancer.Disease models & mechanisms · 2023Article
- Review
- Electrostatic plasma membrane targeting contributes to Dlg function in cell polarity and tumorigenesis.Development (Cambridge, England) · 2021Article
- Genome-Wide Screen for Context-Dependent Tumor Suppressors Identified Using in Vivo Models for Neoplasia inG3 (Bethesda, Md.) · 2020Article
- Two-Faced: Roles of JNK Signalling During Tumourigenesis in theFrontiers in cell and developmental biology · 2020Review
- Role of α-Catenin and its mechanosensing properties in regulating Hippo/YAP-dependent tissue growth.PLoS genetics · 2019Article
- MKK3 modulates JNK-dependent cell migration and invasion.Cell death & disease · 2019Article
- Review
- Prp8 regulates oncogene-induced hyperplastic growth inDevelopment (Cambridge, England) · 2018Article
- A genome-wide Drosophila epithelial tumorigenesis screen identifies Tetraspanin 29Fb as an evolutionarily conserved suppressor of Ras-driven cancer.PLoS genetics · 2018Article
- Mutations in theProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- Grow With the Challenge - Microbial Effects on Epithelial Proliferation, Carcinogenesis, and Cancer Therapy.Frontiers in microbiology · 2018Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
We have shown previously that mutations in the apico-basal cell polarity regulators cooperate with oncogenic Ras (Ras(ACT)) to promote tumorigenesis in Drosophila melanogaster and mammalian cells. To identify novel genes that cooperate with Ras(ACT) in tumorigenesis, we carried out a genome-wide screen for genes that when overexpressed throughout the developing Drosophila eye enhance Ras(ACT)-driven hyperplasia. Ras(ACT)-cooperating genes identified were Rac1 Rho1, RhoGEF2, pbl, rib, and east, which encode cell morphology regulators. In a clonal setting, which reveals genes conferring a competitive advantage over wild-type cells, only Rac1, an activated allele of Rho1 (Rho1(ACT)), RhoGEF2, and pbl cooperated with Ras(ACT), resulting in reduced differentiation and large invasive tumors. Expression of RhoGEF2 or Rac1 with Ras(ACT) upregulated Jun kinase (JNK) activity, and JNK upregulation was essential for cooperation. However, in the whole-tissue system, upregulation of JNK alone was not sufficient for cooperation with Ras(ACT), while in the clonal setting, JNK upregulation was sufficient for Ras(ACT)-mediated tumorigenesis. JNK upregulation was also sufficient to confer invasive growth of Ras(V12)-expressing mammalian MCF10A breast epithelial cells. Consistent with this, HER2(+) human breast cancers (where human epidermal growth factor 2 is overexpressed and Ras signaling upregulated) show a significant correlation with a signature representing JNK pathway activation. Moreover, our genetic analysis in Drosophila revealed that Rho1 and Rac are important for the cooperation of RhoGEF2 or Pbl overexpression and of mutants in polarity regulators, Dlg and aPKC, with Ras(ACT) in the whole-tissue context. Collectively our analysis reveals the importance of the RhoGEF/Rho-family/JNK pathway in cooperative tumorigenesis with Ras(ACT).
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Registered trials
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