ArticleStem cell research & therapy2016
Bile acid: a potential inducer of colon cancer stem cells.
Article in Stem cell research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
102 citing papers in PubMed, 2 syntheses or guidelines pooled it, 166 citations in OpenAlex.
- Use of Dietary Fibers in Reducing the Risk of Several Cancer Types: An Umbrella Review.Nutrients · 2023Pooled it
- Cholecystectomy promotes the development of colorectal cancer by the alternation of bile acid metabolism and the gut microbiota.Frontiers in medicine · 2022Pooled it
- Distinct effects of supplementation with resistant starch and polydextrose on plasma and faecal bile acid profile and associations with gut microbiota: a randomised, controlled intervention in healthy participants.European journal of nutrition · 2026Trial
- Cancer Prevention with Resistant Starch in Lynch Syndrome Patients in the CAPP2-Randomized Placebo Controlled Trial: Planned 10-Year Follow-up.Cancer prevention research (Philadelphia, Pa.) · 2022Trial
- Prevention of colonic neoplasia with polyethylene glycol: A short term randomized placebo-controlled double-blinded trial.PloS one · 2018Trial
- Genome-Guided Probiotic Mechanisms of Enterococcus hirae SMU2502: Wnt/β-catenin-Driven Intestinal Epithelial Proliferation and Protection Against Salmonella Infection.Probiotics and antimicrobial proteins · 2026Article
- The Gut-Adipose-Tumor Axis in Obesity-Related Cancer.Nutrients · 2026Review
- The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026Review
- Interplay Between Gut Microbiota and Cholesterol Metabolism in Colorectal Cancer.International journal of molecular sciences · 2026Review
- Gut microbial metabolites in inflammation-associated colorectal cancer: mechanisms and therapeutic implications.Frontiers in microbiology · 2026Review
- Intestinal pH: a major driver of human gut microbiota composition and metabolism.Nature reviews. Gastroenterology & hepatology · 2025Review
- The Impact of Cholecystectomy on Colorectal Cancer Risk: A Comprehensive Review on Risk Factors and the Association.Current gastroenterology reports · 2025Review
- The Oncogenic Burden of Obesity: Mechanistic Links Between Adiposity and Gastrointestinal Cancers-A Comprehensive Narrative Review.Biomedicines · 2025Review
- Gut Feelings: How Microbes, Diet, and Host Immunity Shape Disease.Biomedicines · 2025Review
- Biological Actions of Bile Acids via Cell Surface Receptors.International journal of molecular sciences · 2025Review
- Untargeted metabolomic profiling for identifying systemic signatures of helicobacter pylori infection in a guinea pig model.Scientific reports · 2025Article
- The Elevation and Impact of Peripheral Bile Acids in Chronic Lymphocytic Leukemia.Biomedicines · 2025Article
- Emerging role of bile acids in colorectal liver metastasis: From molecular mechanism to clinical significance (Review).International journal of oncology · 2025Review
- Yanggan Yizhong decoction prevents liver metastasis from colorectal cancer by targeting myeloid-derived suppressor cells through the regulation of bile acid metabolism in the gut microbiota.Frontiers in microbiology · 2025Article
- Microbiota-derived metabolites in tumorigenesis: mechanistic insights and therapeutic implications.Frontiers in pharmacology · 2025Review
42 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
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAlthough the unconjugated secondary bile acids, specifically deoxycholic acid (DCA) and lithocholic acid (LCA), are considered to be risk factors for colorectal cancer, the precise mechanism(s) by which they regulate carcinogenesis is poorly understood. We hypothesize that the cytotoxic bile acids may promote stemness in colonic epithelial cells leading to generation of cancer stem cells (CSCs) that play a role in the development and progression of colon cancer.
methodsNormal human colonic epithelial cells (HCoEpiC) were used to study bile acid DCA/LCA-mediated induction of CSCs. The expression of CSC markers was measured by real-time qPCR. Flow cytometry was used to isolate CSCs. T-cell factor/lymphoid-enhancing factor (TCF/LEF) luciferase assay was employed to examine the transcriptional activity of β-catenin. Downregulation of muscarinic 3 receptor (M3R) was achieved through transfection of corresponding siRNA.
resultsWe found DCA/LCA to induce CSCs in normal human colonic epithelial cells, as evidenced by the increased proportion of CSCs, elevated levels of several CSC markers, as well as a number of epithelial-mesenchymal transition markers together with increased colonosphere formation, drug exclusion, ABCB1 and ABCG2 expression, and induction of M3R, p-EGFR, matrix metallopeptidases, and c-Myc. Inhibition of M3R signaling greatly suppressed DCA/LCA induction of the CSC marker ALDHA1 and also c-Myc mRNA expression as well as transcriptional activation of TCF/LEF.
conclusionsOur results suggest that bile acids, specifically DCA and LCA, induce cancer stemness in colonic epithelial cells by modulating M3R and Wnt/β-catenin signaling and thus could be considered promoters of colon cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.