ArticleWorld journal of gastrointestinal oncology2024
Bidirectional effects of the tryptophan metabolite indole-3-acetaldehyde on colorectal cancer.
Article in World journal of gastrointestinal oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Amino acid metabolic reprogramming by gut microbiota: a novel metabolic checkpoint in the tumor microenvironment.Gut microbes · 2026Review
- Protocatechuic acid attenuated inflammation caused byVirulence · 2026Article
- Tryptophan metabolism in colorectal cancer: From mechanistic insights to novel therapeutic strategies.Clinical and translational medicine · 2026Review
- Anticancer and Antimicrobial Activity ofMolecules (Basel, Switzerland) · 2026Article
- Association analysis of the differences in intestinal flora and clinical tumor indicators among colorectal cancer patients.Frontiers in cellular and infection microbiology · 2026Article
- Enhancing functional properties and analysis of sugar and metabolite composition ofFood chemistry: X · 2025Article
- Clinical Detection and Management of Colorectal Cancer Concerning the Gut Microbiome.Scientifica · 2025Review
- Microbiota-host metabolism reprogramming in colorectal cancer: from pathogenesis to precision therapies.Frontiers in oncology · 2025Review
- Metabolic interactions: how gut microbial metabolites influence colorectal cancer.Frontiers in microbiology · 2025Review
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6 authors.
Funding
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Abstract
backgroundColorectal cancer (CRC) has a high incidence and mortality. Recent studies have shown that indole derivatives involved in gut microbiota metabolism can impact the tumorigenesis, progression, and metastasis of CRC.
aimTo investigate the effect of indole-3-acetaldehyde (IAAD) on CRC.
methodsThe effect of IAAD was evaluated in a syngeneic mouse model of CRC and CRC cell lines (HCT116 and DLD-1). Cell proliferation was assessed by Ki-67 fluorescence staining and cytotoxicity tests. Cell apoptosis was analysed by flow cytometry after staining with Annexin V-fluorescein isothiocyanate and propidium iodide. Invasiveness was investigated using the transwell assay. Western blotting and real-time fluorescence quantitative polymerase chain reaction were performed to evaluate the expression of epithelial-mesenchymal transition related genes and aryl hydrocarbon receptor (AhR) downstream genes. The PharmMapper, SEA, and SWISS databases were used to screen for potential target proteins of IAAD, and the core proteins were identified through the String database.
resultsIAAD reduced tumorigenesis in a syngeneic mouse model. In CRC cell lines HCT116 and DLD1, IAAD exhibited cytotoxicity starting at 24 h of treatment, while it reduced Ki67 expression in the nucleus. The results of flow cytometry showed that IAAD induced apoptosis in HCT116 cells but had no effect on DLD1 cells, which may be related to the activation of AhR. IAAD can also increase the invasiveness and epithelial-mesenchymal transition of HCT116 and DLD1 cells. At low concentrations (< 12.5 μmol/L), IAAD only exhibited cytotoxic effects without promoting cell invasion. In addition, predictions based on online databases, protein-protein interaction analysis, and molecular docking showed that IAAD can bind to matrix metalloproteinase-9 (MMP9), angiotensin converting enzyme (ACE), poly(ADP-ribose) polymerase-1 (PARP1), matrix metalloproteinase-2 (MMP2), and myeloperoxidase (MPO).
conclusionIndole-3-aldehyde can induce cell apoptosis and inhibit cell proliferation to prevent the occurrence of CRC; however, at high concentrations (≥ 25 μmol/L), it can also promote epithelial-mesenchymal transition and invasion in CRC cells. IAAD activates AhR and directly binds MMP9, ACE, PARP1, MMP2, and MPO, which partly reveals why it has a bidirectional effect.
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