Properties |
Information |
PhytoCAT-ID |
PhytoCAT-1871 |
Phytochemical name or plant extracts |
Corilagin |
PMID |
26935808 |
Literature evidence |
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. |
IUPAC name |
[(1S,19R,21S,22R,23R)-6,7,8,11,12,13,22,23-octahydroxy-3,16-dioxo-2,17,20-trioxatetracyclo[17.3.1.04,9.010,15]tricosa-4,6,8,10,12,14-hexaen-21-yl] 3,4,5-trihydroxybenzoate |
Phytochemicals’ class or type of plant extracts |
Polyphenol tannic acid |
Source of phytochemicals or plant Extracts |
Euphorbia fischeriana |
|
Geographical availability |
China North-Central, Chita, Inner Mongolia, Korea, Manchuria, Mongolia |
Plant parts |
NA |
Other cancers |
Breast cancer, Liver cancer |
Target gene or protein |
Hes1, Notch1, mTOR |
Gene or Protein evidence |
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. |
Target pathways |
NA |
IC50 |
NA |
Potency |
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. |
Cell line/ mice model |
MCF-7, HepG2, CCA |
Additional information |
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. |
PubChem ID |
73568 |
Additional PMIDs |
26935808 30609707 31546767 25556473 |
Additional sources of information |
https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:346510-1 |
Safety |
NA |