ArticleMolecular cancer2015
A functional connectome: regulation of Wnt/TCF-dependent transcription by pairs of pathway activators.
Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- POFUT1 promotes gastric cancer progression through Notch/Wnt dual signaling pathways dependent on the parafibromin-NICD1-β-catenin complex.Journal of the Chinese Medical Association : JCMA · 2023Article
- SEPTIN3 Promotes Progression of Triple-Negative Breast Cancer via Activating Wnt Pathway.International journal of general medicine · 2023Article
- CEMIP, a Promising Biomarker That Promotes the Progression and Metastasis of Colorectal and Other Types of Cancer.Cancers · 2022Review
- Functional Genomics of PRUNE1 in Neurodevelopmental Disorders (NDDs) Tied to Medulloblastoma (MB) and Other Tumors.Frontiers in oncology · 2021Review
- T-Cell Factors as Transcriptional Inhibitors: Activities and Regulations in Vertebrate Head Development.Frontiers in cell and developmental biology · 2021Review
- Integrative analysis of h-prune as a potential therapeutic target for hepatocellular carcinoma.EBioMedicine · 2019Article
- LRP16 prevents hepatocellular carcinoma progression through regulation of Wnt/β-catenin signaling.Journal of molecular medicine (Berlin, Germany) · 2018Article
- Article
- PRUNE is crucial for normal brain development and mutated in microcephaly with neurodevelopmental impairment.Brain : a journal of neurology · 2017Article
- Gene expression and pathway analysis ofWorld journal of stem cells · 2016Article
- Secreted HMGB1 from Wnt activated intestinal cells is required to maintain a crypt progenitor phenotype.Oncotarget · 2016Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundWnt/β-catenin signaling is often portrayed as a simple pathway that is initiated by Wnt ligand at the cell surface leading, via linear series of interactions between 'core pathway' members, to the induction of nuclear transcription from genes flanked by β-catenin/TCF transcription factor binding sites. Wnt/β-catenin signaling is also regulated by a much larger set of 'non-core regulators'. However the relationship between 'non-core regulators' is currently not well understood. Aberrant activation of the pathway has been shown to drive tumorgenesis in a number of different tissues.
methodsMammalian cells engineered to have a partially-active level of Wnt/β-catenin signaling were screened by transfection for proteins that up or down-regulated a mid-level of TCF-dependent transcription induced by transient expression of an activated LRP6 Wnt co-receptor (∆NLRP).
results141 novel regulators of TCF-dependent transcription were identified. Surprisingly, when tested without ∆NLRP activation, most up-regulators failed to alter TCF-dependent transcription. However, when expressed in pairs, 27 % (466/1170) functionally interacted to alter levels of TCF-dependent transcription. When proteins were displayed as nodes connected by their ability to co-operate in the regulation of TCF-dependent transcription, a network of functional interactions was revealed. In this network, 'core pathway' components (Eg. β-catenin, GSK-3, Dsh) were found to be the most highly connected nodes. Activation of different nodes in this network impacted on the sensitivity to Wnt pathway small molecule antagonists.
conclusionsThe 'functional connectome' identified here strongly supports an alternative model of the Wnt pathway as a complex context-dependent network. The network further suggests that mutational activation of highly connected Wnt signaling nodes predisposed cells to further context-dependent alterations in levels of TCF-dependent transcription that may be important during tumor progression and treatment.
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