ArticleCell death discovery2021
Ursodeoxycholic acid suppresses the malignant progression of colorectal cancer through TGR5-YAP axis.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.
- IBD-related inflammatory memory and colorectal cancer: epigenetic mechanisms and microbiome interventions.Frontiers in immunology · 2026Pooled it
- Cholecystectomy promotes the development of colorectal cancer by the alternation of bile acid metabolism and the gut microbiota.Frontiers in medicine · 2022Pooled it
- A novel bile salt hydrolase-producingGut microbes · 2026Article
- The gut microbiome-bile acid-FXR interplay: a pivotal axis in metabolic and gastrointestinal diseases.Gut microbes · 2026Review
- Bile acid signaling in health and disease.Molecular biomedicine · 2026Review
- Advances in Exercise-Mediated Regulation of the Gut Microbiota via the Muscle-Gut Axis: Implications for Tumor Immunity and Treatment Responses.Metabolites · 2026Review
- Gut microbiota in health and disease.Molecular biomedicine · 2026Review
- Role and progression of bile acid metabolism in mediating Th17/Treg homeostasis in inflammatory bowel disease.iScience · 2026Review
- Gut microbial metabolites in colorectal cancer: dual roles in tumorigenesis, immune crosstalk, and therapeutic innovation.Frontiers in cellular and infection microbiology · 2026Review
- Gut microbial metabolites in inflammation-associated colorectal cancer: mechanisms and therapeutic implications.Frontiers in microbiology · 2026Review
- Involvement of bile acids in cholangiocarcinoma progressionWorld journal of gastrointestinal oncology · 2025Article
- Article
- Intestinal dysbiosis and colorectal cancer.Chinese medical journal · 2025Review
- Ginsenoside Rh4 inhibits colorectal cancer via the modulation of gut microbiota-mediated bile acid metabolism.Journal of advanced research · 2025Article
- Crosstalk Between Bile Acids and Intestinal Epithelium: Multidimensional Roles of Farnesoid X Receptor and Takeda G Protein Receptor 5.International journal of molecular sciences · 2025Review
- Emerging role of bile acids in colorectal liver metastasis: From molecular mechanism to clinical significance (Review).International journal of oncology · 2025Review
- The effects of ursodeoxycholic acid on Parkinson's disease, a mechanistic review of the recent evidence.Metabolic brain disease · 2025Review
- Review
- Metabolic interactions: how gut microbial metabolites influence colorectal cancer.Frontiers in microbiology · 2025Review
- Mechanisms and advantages of natural derived small molecule compounds in the prevention and treatment of colorectal cancer: a review.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Hippo/YAP pathway plays an important role in the development of cancers. Previous studies have reported that bile acids can activate YAP (Yes Associated Protein) to promote tumorigenesis and tumor progression. Ursodeoxycholic acid (UDCA) is a long-established old drug used for cholestasis treatment. So far, the effect of UDCA on YAP signaling in colorectal cancer (CRC) is not well defined. This study means to explore relationship of UDCA and YAP in CRC. UDCA suppressed YAP signaling by activating the membrane G-protein-coupled bile acid receptor (TGR5). TGR5 mainly regulated cAMP/PKA signaling pathway to inhibit RhoA activity, thereby suppressing YAP signaling. Moreover, the restoration of YAP expression alleviated the inhibitory effect of UDCA on CRC cell proliferation. In AOM/DSS-induced CRC model, UDCA inhibited tumor growth in a concentration-dependent manner and decreased expression of YAP and Ki67. UDCA plays a distinguished role in regulating YAP signaling and CRC growth from the primary bile acids and partial secondary bile acids, demonstrating the importance of maintaining normal intestinal bile acid metabolism in cancer patients. It also presents a potential therapeutic intervention for CRC.
Identifiers
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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.