ArticleOncogene2015
Contributions of DNA repair, cell cycle checkpoints and cell death to suppressing the DNA damage-induced tumorigenic behavior of Drosophila epithelial cells.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Dual contributions of Xrp1 to genome integrity through the DNA damage response and cell competition.PLoS genetics · 2026Article
- Proteostasis failure and mitochondrial dysfunction contribute to chromosomal instability-induced microcephaly.Nature communications · 2026Article
- mTORC1 inhibition by metformin synergizes with dendrosomal nano-curcumin to induce apoptosis via modulation of pro- and anti-apoptotic proteins in breast cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Rad53 orchestrates divergent pathways governing genotoxic resistance, morphogenesis, and virulence inVirulence · 2025Article
- Control of mitochondrial dynamics by the metabolic regulator dPGC1 limits Yorkie-induced oncogenic growth in Drosophila.PLoS biology · 2025Article
- Replication stress promotes cellular transformation in Drosophila epithelium.Cell death discovery · 2025Article
- Advanced nano-therapeutic delivery of metformin: potential anti-cancer effect against human colon cancer cells through inhibition of GPR75 expression.Medical oncology (Northwood, London, England) · 2023Article
- Control of Cell Growth and Proliferation by the Tribbles Pseudokinase: Lessons from Drosophila.Cancers · 2021Review
- The Impact ofInternational journal of molecular sciences · 2020Article
- Genomic instability and cancer: lessons fromOpen biology · 2020Review
- Genetic mechanisms of formation of radiation-induced instability of the genome and its transgenerational effects in the descendants of chronically irradiated individuals of Drosophila melanogaster.Radiation and environmental biophysics · 2020Article
- RecQL4-Aurora B kinase axis is essential for cellular proliferation, cell cycle progression, and mitotic integrity.Oncogenesis · 2018Article
- Caspases maintain tissue integrity by an apoptosis-independent inhibition of cell migration and invasion.Nature communications · 2018Article
- Modelling Cooperative Tumorigenesis inBioMed research international · 2018Review
- Overexpression of theHereditas · 2018Article
- Epithelial tumors: Growing from within.Fly · 2018Article
- Screening and purification of natural products from actinomycetes that affect the cell shape of fission yeast.Journal of cell science · 2017Article
- MiRNA-binding site functional polymorphisms in DNA repair genes RAD51, RAD52, and XRCC2 and breast cancer risk in Chinese population.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- miR-8 modulates cytoskeletal regulators to influence cell survival and epithelial organization in Drosophila wings.Developmental biology · 2016Article
- Identifying novel protein phenotype annotations by hybridizing protein-protein interactions and protein sequence similarities.Molecular genetics and genomics : MGG · 2016Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When exposed to DNA-damaging agents, components of the DNA damage response (DDR) pathway trigger apoptosis, cell cycle arrest and DNA repair. Although failures in this pathway are associated with cancer development, the tumor suppressor roles of cell cycle arrest and apoptosis have recently been questioned in mouse models. Using Drosophila epithelial cells that are unable to activate the apoptotic program, we provide evidence that ionizing radiation (IR)-induced DNA damage elicits a tumorigenic behavior in terms of E-cadherin delocalization, cell delamination, basement membrane degradation and neoplasic overgrowth. The tumorigenic response of the tissue to IR is enhanced by depletion of Okra/DmRAD54 or spnA/DmRAD51--genes required for homologous recombination (HR) repair of DNA double-strand breaks in G2--and it is independent of the activity of Lig4, a ligase required for nonhomologous end-joining repair in G1. Remarkably, depletion of Grapes/DmChk1 or Mei-41/dATR-genes affecting DNA damage-induced cell cycle arrest in G2--compromised DNA repair and enhanced the tumorigenic response of the tissue to IR. On the contrary, DDR-independent lengthening of G2 had a positive impact on the dynamics of DNA repair and suppressed the tumorigenic response of the tissue to IR. Our results support a tumor suppressor role of apoptosis, DNA repair by HR and cell cycle arrest in G2 in simple epithelia subject to IR-induced DNA damage.
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