Properties |
Information |
PhytoCAT-ID |
PhytoCAT-627 |
Phytochemical name or plant extracts |
AG36 |
PMID |
32643027 |
Literature evidence |
The results indicated that AG36 could significantly inhibit the proliferation, migration and invasion of human umbilical vein endothelial cells (HUVEC). |
IUPAC name |
NA |
Phytochemicals’ class or type of plant extracts |
Triterpenoid saponin |
Source of phytochemicals or plant Extracts |
Ardisia gigantifolia |
|
Geographical availability |
China South-Central, China Southeast, Hainan, Laos, Thailand, Vietnam |
Plant parts |
Rhizome |
Other cancers |
Breast cancer |
Target gene or protein |
Cyclin B1, Cyclin D1, FAK, AKT, VEGF, VEGFR2, Caspase 3, Caspase 8, Bax, Bcl-2, Fas, FasL, TNFR1, DR5, cyt-c |
Gene or Protein evidence |
Moreover, AG36 decreased the protein expression of cycle regulatory proteins cyclin B1 or cyclin D1. Further antiangiogenic molecular mechanism investigation showed that AG36 significantly suppressed phosphorylated FAK and AKT, and downregulated the expressions of vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor 2 (VEGFR2) in HUVECs. In addition, AG36 inhibited the tumor growth in xenograft model and expressions of p-VEGFR2 and p-Akt in vivo.
Moreover, AG36 decreased the protein expression of cycle regulatory proteins cyclin B1 or cyclin D1. In MCF-7 and MDA-MB-231 cells, AG36 strongly increased the cleaved caspase-3 and -8 protein expressions, while in SK-BR-3 cells, AG36 only increased the protein expression of cleaved caspase-3. In all the three breast cancer cells, the ratio of Bax/Bcl-2 and cytosolic cytochrome c content increased significantly compared with control group. The death receptor-related proteins Fas/FasL, TNFR1, and DR5 were detected by Western blot, it showed that different breast cancer cells activated the death receptor-mediated extrinsic caspase-8 pathway through different receptors. |
Target pathways |
NA |
IC50 |
At 48h:
0.73 μM against MCF-7
18.1 μM against MDA-MB-231
3.4 μM against SKBR-3 |
Potency |
Our recent studies proved that AG36 displayed prominent cytotoxicity against breast cancer cells both in vitro and in vivo.
In conclusion, AG36 inhibited MCF-7, MDA-MB-231, and SK-BR-3 cells proliferation by the intrinsic mitochondrial and the extrinsic death receptor pathways and AG36 might be a potential breast cancer therapeutic agent. |
Cell line/ mice model |
MCF-7, MDA-MB-231, SKBR-3, BALB/c nude mice |
Additional information |
NA |
PubChem ID |
NA |
Additional PMIDs |
28184196 32643027 |
Additional sources of information |
https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:587033-1 |
Safety |
NA |