ArticleOncotarget2016
Wnt signalling is a bi-directional vulnerability of cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Meta-analysis identifies key genes and pathways implicated in Benzo[a]pyrene exposure response.Chemosphere · 2024Pooled it
- Integrated transcriptomic profiling reveals immune and molecular stage-specific signatures of colorectal cancer in hispanics living in Puerto Rico.Frontiers in immunology · 2026Article
- The role of Wnt/β-catenin signaling in lung cancer progression and therapy: a comprehensive review.Medical oncology (Northwood, London, England) · 2025Review
- Article
- Crosstalk of the Wnt/β-Catenin Signaling Pathway in the Induction of Apoptosis on Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2021Review
- A Chemo-Genomic Approach Identifies Diverse Epigenetic Therapeutic Vulnerabilities in MYCN-Amplified Neuroblastoma.Frontiers in cell and developmental biology · 2021Article
- Article
- Article
- Article
- Review
- Differential regulation of myc homologs by Wnt/β-Catenin signaling in the early metazoan Hydra.The FEBS journal · 2019Article
- Wnt Signaling Is a Major Determinant of Neuroblastoma Cell Lineages.Frontiers in molecular neuroscience · 2019Article
- Transcriptome 3'end organization by PCF11 links alternative polyadenylation to formation and neuronal differentiation of neuroblastoma.Nature communications · 2018Article
- Article
- Investigating the mechanistic basis of biomechanical input controlling skeletal development: exploring the interplay with Wnt signalling at the joint.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Article
- Wnt Signalling Drives Context-Dependent Differentiation or Proliferation in Neuroblastoma.Neoplasia (New York, N.Y.) · 2018Article
- WNT signaling, the development of the sympathoadrenal-paraganglionic system and neuroblastoma.Cellular and molecular life sciences : CMLS · 2018Review
- Sea turtle fibropapilloma tumors share genomic drivers and therapeutic vulnerabilities with human cancers.Communications biology · 2018Article
- Towards a Unified Understanding of Lithium Action in Basic Biology and its Significance for Applied Biology.The Journal of membrane biology · 2017Review
- Neural crest and cancer: Divergent travelers on similar paths.Mechanisms of development · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wnt signalling is involved in the formation, metastasis and relapse of a wide array of cancers. However, there is ongoing debate as to whether activation or inhibition of the pathway holds the most promise as a therapeutic treatment for cancer, with conflicting evidence from a variety of tumour types. We show that Wnt/β-catenin signalling is a bi-directional vulnerability of neuroblastoma, malignant melanoma and colorectal cancer, with hyper-activation or repression of the pathway both representing a promising therapeutic strategy, even within the same cancer type. Hyper-activation directs cancer cells to undergo apoptosis, even in cells oncogenically driven by β-catenin. Wnt inhibition blocks proliferation of cancer cells and promotes neuroblastoma differentiation. Wnt and retinoic acid co-treatments synergise, representing a promising combination treatment for MYCN-amplified neuroblastoma. Additionally, we report novel cross-talks between MYCN and β-catenin signalling, which repress normal β-catenin mediated transcriptional regulation. A β-catenin target gene signature could predict patient outcome, as could the expression level of its DNA binding partners, the TCF/LEFs. This β-catenin signature provides a tool to identify neuroblastoma patients likely to benefit from Wnt-directed therapy. Taken together, we show that Wnt/β-catenin signalling is a bi-directional vulnerability of a number of cancer entities, and potentially a more broadly conserved feature of malignant cells.
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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.