ArticleMolecular biology of the cell2004
Deoxycholic acid activates beta-catenin signaling pathway and increases colon cell cancer growth and invasiveness.
Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 2 of them syntheses that pooled it.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
99 citing papers in PubMed, 2 syntheses or guidelines pooled it, 177 citations in OpenAlex.
- The Clinical Impact of Time-restricted Eating on Cancer: A Systematic Review.Nutrition reviews · 2025Pooled it
- Cholecystectomy promotes the development of colorectal cancer by the alternation of bile acid metabolism and the gut microbiota.Frontiers in medicine · 2022Pooled it
- Bile Acid Metabolism as a Unifying Readout for Diet, Microbiome Function, and Gastrointestinal Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Secondary bile acid production by gut bacteria promotes Western diet-associated colorectal cancer.Gut · 2026Article
- Captivating Synergistic, Dose-Dependent Anticancer Effects of Tumor-Regulation Modulators Chloroquine and Ivermectin Completely Abolished by an Opposing Modulator, Deoxycholic Acid, in Hamster Fibrosarcoma: In Vivo, In Vitro, and Literature Review.Pharmaceuticals (Basel, Switzerland) · 2026Article
- The intricate interplay of microbial metabolomics and carcinogenesis: a spotlight on mechanistic pathways, clinical implications and methodological challenges.Frontiers in cellular and infection microbiology · 2026Review
- Gut microbial metabolites in inflammation-associated colorectal cancer: mechanisms and therapeutic implications.Frontiers in microbiology · 2026Review
- Untargeted Metabolomics Reveals Metabolic Reprogramming Linked to HCC Risk in Late Diagnosed Tyrosinemia Type 1.Metabolites · 2025Article
- Three-Dimensional Culture of Epithelial Cells on Electrospun Nanofibrous Scaffolds.International journal of molecular sciences · 2025Review
- High-fat diet driven post-operative colon cancer recurrence is dependent upon genetic susceptibility to deoxycholic acid.Cancer letters · 2025Article
- Multifaceted roles of microbiota-derived deoxycholic acid in gastrointestinal cancers: from barrier disruption to therapeutic implications.Human cell · 2025Review
- Interactions Between Dietary Metabolites and Regulatory Risk Variants for Human Colon Cancer.bioRxiv : the preprint server for biology · 2025Article
- The microbiome-cancer axis as a hidden contributor to early-onset tumorigenesis.Medical oncology (Northwood, London, England) · 2025Review
- Biological functions and pharmacological behaviors of bile acids in metabolic diseases.Journal of advanced research · 2025Review
- Article
- Emerging role of bile acids in colorectal liver metastasis: From molecular mechanism to clinical significance (Review).International journal of oncology · 2025Review
- Faecalcrobiota metabolites: emerging insights into cancer radiotherapy outcomes.Frontiers in microbiology · 2025Review
- Multi-omics analysis revealed significant metabolic changes in brain cancer cells treated with paclitaxel and/or topotecan.Heliyon · 2024Article
- The human microbiome in space: parallels between Earth-based dysbiosis, implications for long-duration spaceflight, and possible mitigation strategies.Clinical microbiology reviews · 2024Review
- A Narrative Review: Immunometabolic Interactions of Host-Gut Microbiota and Botanical Active Ingredients in Gastrointestinal Cancers.International journal of molecular sciences · 2024Review
39 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer is often lethal when invasion and/or metastasis occur. Tumor progression to the metastatic phenotype is mainly dependent on tumor cell invasiveness. Secondary bile acids, particularly deoxycholic acid (DCA), are implicated in promoting colon cancer growth and progression. Whether DCA modulates beta-catenin and promotes colon cancer cell growth and invasiveness remains unknown. Because beta-catenin and its target genes urokinase-type plasminogen activator receptor (uPAR) and cyclin D1 are overexpressed in colon cancers, and are linked to cancer growth, invasion, and metastasis, we investigated whether DCA activates beta-catenin signaling and promotes colon cancer cell growth and invasiveness. Our results show that low concentrations of DCA (5 and 50 microM) significantly increase tyrosine phosphorylation of beta-catenin, induce urokinase-type plasminogen activator, uPAR, and cyclin D1 expression and enhance colon cancer cell proliferation and invasiveness. These events are associated with a substantial loss of E-cadherin binding to beta-catenin. Inhibition of beta-catenin with small interfering RNA significantly reduced DCA-induced uPAR and cyclin D1 expression. Blocking uPAR with a neutralizing antibody significantly suppressed DCA-induced colon cancer cell proliferation and invasiveness. These findings provide evidence for a novel mechanism underlying the oncogenic effects of secondary bile acids.
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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.