ArticleCarcinogenesis2010
The intestine-specific transcription factor Cdx2 inhibits beta-catenin/TCF transcriptional activity by disrupting the beta-catenin-TCF protein complex.
Article in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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
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Who cites it
49 citing papers in PubMed, 70 citations in OpenAlex.
- CDX2-UPK1B-PIK3IP1-PI3K/AKT signaling axis regulates gastric cancer cell invasion and migration and influences patient prognosis.Experimental and therapeutic medicine · 2026Article
- CDX2 confers ferroptosis resistance in stage II-III colon cancer via upregulation of NUPR1.Cell death & disease · 2026Article
- CANDiT: A machine learning framework for differentiation therapy in colorectal cancer.Cell reports. Medicine · 2025Article
- CDX2 downregulation regulates intrinsic WNT pathway activation, dictating metastasis in APC and CTNNB1 wildtype colorectal cancer.Oncogene · 2025Article
- CDX1 and CDX2 suppress colon cancer stemness by inhibiting β-catenin-facilitated formation of Pol II-DSIF-PAF1C complex.Cell death & disease · 2025Article
- Article
- High-fat diet plus HNF1A variant promotes polyps by activating β-catenin in early-onset colorectal cancer.JCI insight · 2023Article
- Mitochondrial translocator protein deficiency exacerbates pathology in acute experimental ulcerative colitis.Frontiers in physiology · 2022Article
- LINC01419-mediated epigenetic silencing of ZIC1 promotes metastasis in hepatocellular carcinoma through the PI3K/Akt signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Article
- CDX2 expression and perioperative patient serum affects the adhesion properties of cultured colon cancer cells.BMC cancer · 2020Article
- ARE CDX2, BETA-CATENIN AND WNT IMMUNOMARCHERS USEFUL FOR EVALUATING THE CHANCE OF DISEASE PROGRESSION OR EVOLUTION TO DEATH IN PATIENTS WITH COLORECTAL CANCER?Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgery · 2020Article
- Intestinal Neurod1 expression impairs paneth cell differentiation and promotes enteroendocrine lineage specification.Scientific reports · 2019Article
- The Tumor Microenvironment in Colorectal Cancer Therapy.Cancers · 2019Review
- HNF4α and CDX2 Regulate IntestinalInternational journal of molecular sciences · 2019Article
- CDX2 inhibits the proliferation and tumor formation of colon cancer cells by suppressing Wnt/β-catenin signaling via transactivation of GSK-3β and Axin2 expression.Cell death & disease · 2019Article
- Potential signaling pathways as therapeutic targets for overcoming chemoresistance in mucinous ovarian cancer.Biomedical reports · 2018Article
- Degree of Tissue Differentiation Dictates Susceptibility to BRAF-Driven Colorectal Cancer.Cell reports · 2017Article
- Fine-tuning and autoregulation of the intestinal determinant and tumor suppressor homeobox gene CDX2 by alternative splicing.Cell death and differentiation · 2017Article
- CDX2 Stimulates the Proliferation of Porcine Intestinal Epithelial Cells by Activating the mTORC1 and Wnt/β-Catenin Signaling Pathways.International journal of molecular sciences · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cdx2 is an intestine-specific transcription factor known to regulate proliferation and differentiation. We have reported previously that Cdx2 limits the proliferation of human colon cancer cells by inhibiting the transcriptional activity of the beta-catenin-T-cell factor (TCF) bipartite complex. Herein we further elucidate this mechanism. Studies with a classic Cdx2 target gene and a canonical Wnt/beta-catenin/TCF reporter suggest that Cdx2 regulates these promoters by distinctly different processes. Specifically, inhibition of beta-catenin/TCF activity by Cdx2 does not require Cdx2 transcriptional activity. Instead, Cdx2 binds beta-catenin and disrupts its interaction with the DNA-binding TCF factors, thereby silencing beta-catenin/TCF target gene expression. Using Cdx2 mutants, we map the Cdx2 domains required for the inhibition of beta-catenin/TCF activity. We identify a subdomain in the N-terminus that is highly conserved and when mutated significantly reduces Cdx2 inhibition of beta-catenin/TCF transcriptional activity. Mutation of this subdomain also abrogates Cdx2's anti-proliferative effects in colon cancer cells. In summary, we conclude that Cdx2 binds beta-catenin and disrupts the beta-catenin-TCF complex. Considering the pivotal role of beta-catenin/TCF activity in driving proliferation of normal intestinal epithelial and colon cancer cells, our findings suggest a novel mechanism for Cdx2-mediated regulation of Wnt/beta-catenin signaling and cell proliferation.
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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.