ArticleInternational journal of oncology2016
Corilagin suppresses cholangiocarcinoma progression through Notch signaling pathway in vitro and in vivo.
Article in International journal of oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- How to efficiently establish animal models of cholangiocarcinoma: challenges and inspiration.Medical review (2021) · 2026Review
- Corilagin induces apoptosis in glioblastoma cells by disrupting metabolic homeostasis: a metabolomics perspective.Die Naturwissenschaften · 2026Article
- Corilagin induces pyroptosis in AML cells by activating the TXNIP-caspase-3-GSDME pathway.Annals of hematology · 2026Article
- Corilagin enhances the anti-tumor activity of 5-FU by downregulating the expression of GRP 78.Scientific reports · 2023Article
- Atractylodin and β-eudesmol from Atractylodes lancea (Thunb.) DC. Inhibit Cholangiocarcinoma Cell Proliferation by Downregulating the Notch Signaling Pathway.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Notch signaling in the pathogenesis, progression and identification of potential targets for cholangiocarcinoma (Review).Molecular and clinical oncology · 2022Review
- Corilagin prevents non-alcoholic fatty liver diseaseFrontiers in nutrition · 2022Article
- A systems pharmacology approach to identify the autophagy-inducing effects of Traditional Persian medicinal plants.Scientific reports · 2021Article
- Notch signalling pathway in development of cholangiocarcinoma.World journal of gastrointestinal oncology · 2020Review
- Corilagin Ameliorates Atherosclerosis in Peripheral Artery Disease via the Toll-Like Receptor-4 Signaling PathwayFrontiers in immunology · 2020Article
- Corilagin in Cancer: A Critical Evaluation of Anticancer Activities and Molecular Mechanisms.Molecules (Basel, Switzerland) · 2019Review
- Corilagin induces apoptosis, autophagy and ROS generation in gastric cancer cells in vitro.International journal of molecular medicine · 2019Article
- Corilagin Induces High Levels of Apoptosis in the Temozolomide-Resistant T98G Glioma Cell Line.Oncology research · 2018Article
- Corilagin inhibits breast cancer growth via reactive oxygen species-dependent apoptosis and autophagy.Journal of cellular and molecular medicine · 2018Article
- Inhibition of Notch-1 pathway is involved in rottlerin-induced tumor suppressive function in nasopharyngeal carcinoma cells.Oncotarget · 2017Article
- Corilagin relieves atherosclerosis via the toll-like receptor 4 signaling pathway in vascular smooth muscle cells.International journal of immunopathology and pharmacologyArticle
- Antitumor effects of polyphenol-rich extract ofIndian journal of pharmacologyArticle
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Corilagin is a natural plant polyphenol tannic acid with antitumor, anti-inflammatory, and anti-oxidative properties. However, the mechanisms of its actions are largely unknown. Our group reported that corilagin could induce cell inhibition in human breast cancer cell line MCF-7 and human liver hepatocellular carcinoma cell lines HepG2. We report here that corilagin inhibits cholangiocarcinoma (CCA) development through regulating Notch signaling pathway. We found that, in vitro, corilagin inhibited CCA cell proliferation, migration and invasion, promoted CCA cell apoptosis, and inhibited Notch1 and Notch signaling pathway protein expression. Co-immunoprecipitation was used to establish Notch intracellular domain (NICD) interaction with MAML1 and P300 in CCA. Importantly, corilagin reduced Hes1 mRNA level through inhibiting Hes1 promoter activity. In nude mice, corilagin inhibited CCA growth and repressed the expression of Notch1 and mTOR. These results indicate that corilagin may control CCA cell growth by downregulating the expression of Notch1. Therefore, our findings suggest that corilagin may have the potential to become a new therapeutic drug for human CCA.
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