ArticleScientific reports2019
β-catenin activation down-regulates cell-cell junction-related genes and induces epithelial-to-mesenchymal transition in colorectal cancers.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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91 citing papers in PubMed, 127 citations in OpenAlex.
- Targeting JOSD2 degrades β-catenin to suppress colorectal cancer metastasis by disrupting RAS/ERK/β-catenin axis.Acta pharmacologica Sinica · 2026Article
- Syndesmos functions as a tumor suppressor by facilitating epithelial cell adhesion mediated by interactions of E-cadherin and β-catenin.Cell death & disease · 2026Article
- ANO1 stabilizes partial EMT to drive colorectal cancer metastasis through PI3K/AKT/mTOR and ERK signaling pathways.Scientific reports · 2026Article
- CLDN7: Epithelial gatekeeper from physiology to pathology‑roles in cancer and epithelial‑related diseases (Review).International journal of molecular medicine · 2026Review
- AKAP12-LMOD1 signaling defines stromal CAF activation and epithelial junction loss in colorectal cancer.Scientific reports · 2026Article
- From SNPs to pathways: a genome-wide benchmark of annotation discrepancies and their impact on protein- and pathway-level inference.BMC genomics · 2026Article
- Protein buffering of aneuploidy is driven by coordinated factors identified through machine learning.Molecular systems biology · 2026Article
- Tumor-infiltrating bacteria disrupt cancer epithelial cell interactions and induce cell-cycle arrest.Cancer cell · 2026Article
- Copper modulates cell fate through the PLK1-FOXO3a-β-catenin signaling pathway by differentially regulating cuproptosis and EMT.Apoptosis : an international journal on programmed cell death · 2026Article
- SLC41A2 Suppresses Colon Cancer Progression by Inhibiting GSK3β Ubiquitin-proteasome Degradation.Current molecular medicine · 2026Article
- Epigenetic alterations in cancer metastasis: molecular mechanisms and implications for precision oncology.Frontiers in oncology · 2026Review
- Regulation of glypican 6-mediated Wnt activation maintains TDP-43 nuclear localization in neurons.Scientific reports · 2025Article
- Two Sides of the Same Coin-Mechanistic Insight, Diagnostic Application and Therapeutic Translation of Bacterial and Host-Derived Extracellular Vesicles.Journal of extracellular biology · 2025Review
- Regulation of Glypican 6-mediated Wnt activation maintains TDP-43 nuclear localization in neurons.bioRxiv : the preprint server for biology · 2025Article
- Evolutionary conservation and cancer implications of the WNT signaling pathway.Medical oncology (Northwood, London, England) · 2025Review
- TIM3Cancer cell · 2025Article
- Tumor Organoids Grown in Mixed-Composition Hydrogels Recapitulate the Plasticity of Pancreatic Cancers.Gels (Basel, Switzerland) · 2025Article
- Blocking the functional domain of cancer cell surface TIP1 upregulates Midkine via the β-catenin/Wnt signaling pathway.Cancer gene therapy · 2025Article
- Investigation of three alternative histopathological scoring methods at the invasive tumour front in colorectal cancer.The journal of pathology. Clinical research · 2025Article
- Mechanistic insights into epithelial-mesenchymal transition mediated cisplatin resistance in ovarian cancer.Scientific reports · 2025Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
WNT signaling activation in colorectal cancers (CRCs) occurs through APC inactivation or β-catenin mutations. Both processes promote β-catenin nuclear accumulation, which up-regulates epithelial-to-mesenchymal transition (EMT). We investigated β-catenin localization, transcriptome, and phenotypic differences of HCT116 cells containing a wild-type (HCT116-WT) or mutant β-catenin allele (HCT116-MT), or parental cells with both WT and mutant alleles (HCT116-P). We then analyzed β-catenin expression and associated phenotypes in CRC tissues. Wild-type β-catenin showed membranous localization, whereas mutant showed nuclear localization; both nuclear and non-nuclear localization were observed in HCT116-P. Microarray analysis revealed down-regulation of Claudin-7 and E-cadherin in HCT116-MT vs. HCT116-WT. Claudin-7 was also down-regulated in HCT116-P vs. HCT116-WT without E-cadherin dysregulation. We found that ZEB1 is a critical EMT factor for mutant β-catenin-mediated loss of E-cadherin and Claudin-7 in HCT116-P and HCT116-MT cells. We also demonstrated that E-cadherin binds to both WT and mutant β-catenin, and loss of E-cadherin releases β-catenin from the cell membrane and leads to its degradation. Alteration of Claudin-7, as well as both Claudin-7 and E-cadherin respectively caused tight junction (TJ) impairment in HCT116-P, and dual loss of TJs and adherens junctions (AJs) in HCT116-MT. TJ loss increased cell motility, and subsequent AJ loss further up-regulated that. Immunohistochemistry analysis of 101 CRCs revealed high (14.9%), low (52.5%), and undetectable (32.6%) β-catenin nuclear expression, and high β-catenin nuclear expression was significantly correlated with overall survival of CRC patients (P = 0.009). Our findings suggest that β-catenin activation induces EMT progression by modifying cell-cell junctions, and thereby contributes to CRC aggressiveness.
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