ArticlePLoS genetics2018
Signalling crosstalk during early tumorigenesis in the absence of Polycomb silencing.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Epigenetic Regulation in Drosophila Tumor Models.Advances in experimental medicine and biology · 2025Review
- Article
- Polycomb safeguards imaginal disc specification through control of the Vestigial-Scalloped complex.Development (Cambridge, England) · 2023Article
- Mutual repression between JNK/AP-1 and JAK/STAT stratifies senescent and proliferative cell behaviors during tissue regeneration.PLoS biology · 2023Article
- Polycomb safeguards imaginal disc specification through control of the Vestigial-Scalloped complex.bioRxiv : the preprint server for biology · 2023Article
- Size compensation inFrontiers in cell and developmental biology · 2023Article
- Non-apoptotic activation of Drosophila caspase-2/9 modulates JNK signaling, the tumor microenvironment, and growth of wound-like tumors.Cell reports · 2022Article
- Ursolic Acid Protects Sodium Dodecyl Sulfate-InducedAntioxidants (Basel, Switzerland) · 2022Article
- Tumorigenesis and cell competition inProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- PHF19 inhibition as a therapeutic target in multiple myeloma.Current research in translational medicine · 2021Article
- Cell-to-cell communication mediates glioblastoma progression inBiology open · 2020Article
- Rounding up the Usual Suspects: Assessing Yorkie, AP-1, and Stat Coactivation in Tumorigenesis.International journal of molecular sciences · 2020Article
- Two-Faced: Roles of JNK Signalling During Tumourigenesis in theFrontiers in cell and developmental biology · 2020Review
- PHF19 promotes multiple myeloma tumorigenicity through PRC2 activation and broad H3K27me3 domain formation.Blood · 2019Article
- Polycomb and Notch signaling regulate cell proliferation potential duringLife science alliance · 2019Article
- Unscheduled HDAC4 repressive activity in human fibroblasts triggers TP53-dependent senescence and favors cell transformation.Molecular oncology · 2018Article
- A switch in transcription and cell fate governs the onset of an epigenetically-deregulated tumor ineLife · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
In response to stress and injury a coordinated activation of conserved signalling modules, such as JNK and JAK/STAT, is critical to trigger regenerative tissue restoration. While these pathways rebuild homeostasis and promote faithful organ recovery, it is intriguing that they also become activated in various tumour conditions. Therefore, it is crucial to understand how similar pathways can achieve context-dependent functional outputs, likely depending on cellular states. Compromised chromatin regulation, upon removal of the Polycomb group member polyhomeotic, leads to tumour formation with ectopic activation of JNK signalling, mediated by egr/grnd, in addition to JAK/STAT and Notch. Employing quantitative analyses, we show that blocking ectopic signalling impairs ph tumour growth. Furthermore, JAK/STAT functions in parallel to JNK, while Notch relies on JNK. Here, we reveal a signalling hierarchy in ph tumours that is distinct from the regenerative processes regulated by these pathways. Absence of ph renders a permissive state for expression of target genes, but our results suggest that both loss of repression and the presence of activators may collectively regulate gene expression during tumorigenesis. Further dissecting the effect of signalling, developmental or stress-induced factors will thus elucidate the regulation of physiological responses and the contribution of context-specific cellular states.
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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 Socratic graph.