ArticlePLoS genetics2014
Brg1 loss attenuates aberrant wnt-signalling and prevents wnt-dependent tumourigenesis in the murine small intestine.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- The metabolic addiction of cancer stem cells.Frontiers in oncology · 2022Pooled it
- DDOST mediates cervical cancer cell malignant progression by interacting with SMARCA4.American journal of cancer research · 2026Article
- The TRIP12 E3 ligase induces SWI/SNF component BRG1-β-catenin interaction to promote Wnt signaling.Nature communications · 2025Article
- AMBRA1 promotes intestinal inflammation by antagonizing PP4R1/PP4c mediated IKK dephosphorylation in an autophagy-independent manner.Cell death and differentiation · 2024Article
- Epigenetic Activation of Tensin 4 Promotes Gastric Cancer Progression.Molecules and cells · 2023Article
- Sex- and Co-Mutation-Dependent Prognosis in Patients with SMARCA4-Mutated Malignancies.Cancers · 2023Article
- PRMT1-mediated H4R3me2a recruits SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling.Genome medicine · 2021Article
- Compensation between Wnt-driven tumorigenesis and cellular responses to ribosome biogenesis inhibition in the murine intestinal epithelium.Cell death and differentiation · 2020Article
- Epigenetic Regulation of a Disintegrin and Metalloproteinase (ADAM) Transcription in Colorectal Cancer Cells: Involvement of β-Catenin, BRG1, and KDM4.Frontiers in cell and developmental biology · 2020Article
- An Underlying Mechanism of Dual Wnt Inhibition and AMPK Activation: Mitochondrial Uncouplers Masquerading as Wnt Inhibitors.Journal of medicinal chemistry · 2019Article
- BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration.Nature communications · 2019Article
- ARID1A facilitates KRAS signaling-regulated enhancer activity in an AP1-dependent manner in colorectal cancer cells.Clinical epigenetics · 2019Article
- Chromatin remodeling ATPase BRG1 and PTEN are synthetic lethal in prostate cancer.The Journal of clinical investigation · 2019Article
- DNA Methylation Readers and Cancer: Mechanistic and Therapeutic Applications.Frontiers in oncology · 2019Review
- Exome-wide somatic mutation characterization of small bowel adenocarcinoma.PLoS genetics · 2018Article
- Defining key concepts of intestinal and epithelial cancer biology through the use of mouse models.Carcinogenesis · 2017Review
- The BRG1 ATPase of human SWI/SNF chromatin remodeling enzymes as a driver of cancer.Epigenomics · 2017Review
- Article
- Cdx2 Regulates Gene Expression through Recruitment of Brg1-associated Switch-Sucrose Non-fermentable (SWI-SNF) Chromatin Remodeling Activity.The Journal of biological chemistry · 2017Article
- The chromatin-remodeling enzyme BRG1 promotes colon cancer progression via positive regulation of WNT3A.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
Tumourigenesis within the intestine is potently driven by deregulation of the Wnt pathway, a process epigenetically regulated by the chromatin remodelling factor Brg1. We aimed to investigate this interdependency in an in vivo setting and assess the viability of Brg1 as a potential therapeutic target. Using a range of transgenic approaches, we deleted Brg1 in the context of Wnt-activated murine small intestinal epithelium. Pan-epithelial loss of Brg1 using VillinCreERT2 and AhCreERT transgenes attenuated expression of Wnt target genes, including a subset of stem cell-specific genes and suppressed Wnt-driven tumourigenesis improving animal survival. A similar increase in survival was observed when Wnt activation and Brg1 loss were restricted to the Lgr5 expressing intestinal stem cell population. We propose a mechanism whereby Brg1 function is required for aberrant Wnt signalling and ultimately for the maintenance of the tumour initiating cell compartment, such that loss of Brg1 in an Apc-deficient context suppresses adenoma formation. Our results highlight potential therapeutic value of targeting Brg1 and serve as a proof of concept that targeting the cells of origin of cancer may be of therapeutic relevance.
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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.