ArticlePharmaceuticals (Basel, Switzerland)2024
Chlorogenic Acid as a Potential Therapeutic Agent for Cholangiocarcinoma.
Article in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Induction of senescence like macrophages by hepatocellular carcinoma cells in vitro.Discover oncology · 2026Article
- Article
- Preventive Effect of Upland Pigmented Potatoes Against LPS-Induced Inflammation in THP-1 Macrophages.Molecular nutrition & food research · 2025Article
- Research Advances in the Synthesis, Metabolism, and Function of Chlorogenic Acid.Foods (Basel, Switzerland) · 2025Review
- Coffee Wastes: A Sustainable Source of Natural Compounds Suppressing Colorectal Cancer Cell Viability.Oxidative medicine and cellular longevity · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Chlorogenic acid (CGA) has demonstrated anti-tumor effects across various cancers, but its role in cholangiocarcinoma (CCA) remains unclear. Our study revealed CGA's potent anti-tumor effects on CCA, significantly suppressing cell proliferation, migration, colony formation, and invasion while inhibiting the epithelial-mesenchymal transition. CGA induced apoptosis, modulated cell cycle progression, and exhibited a stable binding affinity to AKR1B10 in CCA. AKR1B10 was highly expressed in RBE cells, and CGA treatment reduced AKR1B10 expression. Knocking out AKR1B10 inhibited the proliferation of RBE cells, whereas the overexpression of AKR1B10 promoted their proliferation. Additionally, CGA suppressed the proliferation of RBE cells with AKR1B10 overexpression. Mechanistically, AKR1B10 activated AKT, and CGA exerted its inhibitory effect by reducing AKR1B10 levels, thereby suppressing AKT activation. Furthermore, CGA facilitated the polarization of tumor-associated macrophages towards an anti-tumor phenotype and enhanced T-cell cytotoxicity. These findings underscore CGA's potential as a promising therapeutic agent for CCA treatment.
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Registered trials
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