ArticleNature communications2018
An intrinsic tumour eviction mechanism in Drosophila mediated by steroid hormone signalling.
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 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Psc and Su(z)2 safeguard intestinal stem cell identity and prevent chinmo-dependent tumorigenesis.EMBO reports · 2026Article
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- Temporal neuronal differentiation programs safeguard neuronal diversity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Epigenetic Regulation in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- Nuclear receptor E75/NR1D2 promotes tumor malignant transformation by integrating Hippo and Notch pathways.The EMBO journal · 2024Article
- Tumor elimination by clustered microRNAs miR-306 and miR-79 via noncanonical activation of JNK signaling.eLife · 2022Article
- Non-autonomous regulation of neurogenesis by extrinsic cues: aOxford open neuroscience · 2022Review
- Tumor models in various Drosophila tissues.WIREs mechanisms of disease · 2021Review
- Next-Generation Sequencing Reveals Increased Anti-oxidant Response and Ecdysone Signaling in STAT Supercompetitors inG3 (Bethesda, Md.) · 2019Article
- Developmental regulation of regenerative potential in Drosophila by ecdysone through a bistable loop of ZBTB transcription factors.PLoS biology · 2019Article
Corrections and comments
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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
Polycomb group proteins are epigenetic regulators maintaining transcriptional memory during cellular proliferation. In Drosophila larvae, malfunction of Polyhomeotic (Ph), a member of the PRC1 silencing complex, results in neoplastic growth. Here, we report an intrinsic tumour suppression mechanism mediated by the steroid hormone ecdysone during metamorphosis. Ecdysone alters neoplastic growth into a nontumorigenic state of the mutant ph cells which then become eliminated during adult stage. We demonstrate that ecdysone exerts this function by inducing a heterochronic network encompassing the activation of the microRNA lethal-7, which suppresses its target gene chronologically inappropriate morphogenesis. This pathway can also promote remission of brain tumours formed in brain tumour mutants, revealing a restraining of neoplastic growth in different tumour types. Given the conserved role of let-7, the identification and molecular characterization of this innate tumour eviction mechanism in flies might provide important clues towards the exploitation of related pathways for human tumour therapy.
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