ArticleGastroenterology2017
SPDEF Induces Quiescence of Colorectal Cancer Cells by Changing the Transcriptional Targets of β-catenin.
Article in Gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Phosphatidylinositol 3-Kinase Signaling Enhances Intestinal Crypt Epithelial Cell Recovery after Radiation.The American journal of pathology · 2025Article
- Single-Cell Profiling Reveals Conserved Differentiation and Partial EMT Programs Orchestrating Ecosystem-Level Antagonisms in Head and Neck Cancer.Journal of cellular and molecular medicine · 2025Article
- Eurycomalactone switched hepatocellular carcinoma cells into quiescence through 5'tRFScientific reports · 2025Article
- CircMVP promotes METTL3 activation mediated CTNNB1 m6A modification in the inhibition of colorectal cancer in B7-H3 dependence antitumor immunity.International journal of biological sciences · 2025Article
- ETS-1 in tumor immunology: implications for novel anti-cancer strategies.Frontiers in immunology · 2025Review
- SPDEF drives pancreatic adenocarcinoma progression via transcriptional upregulation ofBiomolecules & biomedicine · 2024Article
- In-vivo screening implicates endoribonuclease Regnase-1 in modulating senescence-associated lysosomal changes.GeroScience · 2024Article
- TSP50 Attenuates DSS-Induced Colitis by Regulating TGF-β Signaling Mediated Maintenance of Intestinal Mucosal Barrier Integrity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- Lipogenesis promotes mitochondrial fusion and maintains cancer stemness in human NSCLC.JCI insight · 2023Article
- TCF7L1 RegulatesGenes · 2023Article
- Intestinal epithelium-specific Fut2 deficiency promotes colorectal cancer through down-regulating fucosylation of MCAM.Journal of translational medicine · 2023Article
- Immune-Related Biomarkers Associated with Lung Metastasis from the Colorectal Cancer Microenvironment.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Article
- Regulatory effect between HMGA2 and the Wnt/β-catenin signaling pathway in the carcinogenesis of sporadic colorectal tubular adenoma.Oncology letters · 2021Article
- Involvement of CDK11B-mediated SPDEF ubiquitination and SPDEF-mediated microRNA-448 activation in the oncogenicity and self-renewal of hepatocellular carcinoma stem cells.Cancer gene therapy · 2021Article
- SPDEF suppresses head and neck squamous cell carcinoma progression by transcriptionally activating NR4A1.International journal of oral science · 2021Article
- A CRISPR/Cas9-EngineeredCancer discovery · 2021Article
- GOLM1 restricts colitis and colon tumorigenesis by ensuring Notch signaling equilibrium in intestinal homeostasis.Signal transduction and targeted therapy · 2021Article
- Stem cell quiescence and its clinical relevance.World journal of stem cells · 2020Review
- Neuroplastinβ-mediated upregulation of solute carrier family 22 member 18 antisense (SLC22A18AS) plays a crucial role in the epithelial-mesenchymal transition, leading to lung cancer cells' enhanced motility.Biochemistry and biophysics reports · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsThe canonical Wnt signaling pathway activates the transcriptional activity of β-catenin. This pathway is often activated in colorectal cancer cells, but strategies to block it in tumors have not been effective. The SAM pointed domain containing ETS transcription factor (SPDEF) suppresses formation of colon tumors by unclear mechanisms. We investigated these mechanisms and the effects of SPDEF on β-catenin activity in mouse models of colorectal cancer (CRC), CRC cell lines, and mouse and human normal and cancer colonoids.
methodsWe performed studies of Lgr5
resultsExpression of SPDEF was sufficient to inhibit intestinal tumorigenesis by activated β-catenin, block tumor cell proliferation, and restrict growth of established tumors. In tumor cells with activated β -catenin, expression of SPDEF induced a quiescent state, which was reversed when SPDEF expression was stopped. In mouse and human normal and tumor-derived enteroids/colonoids, those that expressed SPDEF for 3 days were significantly smaller. SPDEF inhibited the transcriptional activity of β-catenin via a protein-protein interaction, independent of SPDEF DNA binding capacity. SPDEF disrupted β-catenin binding to TCF1 and TCF3, displacing β-catenin from enhancer regions of genes that regulate the cell cycle but not genes that regulate stem cell activities.
conclusionsIn studies of mice and human CRC, we found that SPDEF induces a quiescent state in CRC cells by disrupting binding of β-catenin to TCF1 and TCF3 and regulation of genes that control the cell cycle. In this model, β-catenin activity determines the proliferation or quiescence of CRC cells based on the absence or presence of SPDEF.
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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.