| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-687 | |
| Phytochemical name or plant extracts | Esculentoside A | |
| PMID | 30080291 | |
| Literature evidence | EsA inhibited breast CSC growth in vitro and in vivo through stemness attenuation and apoptosis induction by blocking IL-6/STAT3 signaling pathway, it might serve as a novel candidate agent for human breast cancer treatment and/or prevention. © 2018 John Wiley & Sons, Ltd. | |
| IUPAC name | 10-[3,4-dihydroxy-5-[3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxan-2-yl]oxy-11-hydroxy-9-(hydroxymethyl)-2-methoxycarbonyl-2,6a,6b,9,12a-pentamethyl-1,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic acid | |
| Phytochemicals’ class or type of plant extracts | Triterpenoid saponin | |
| Source of phytochemicals or plant Extracts | Phytolacca acinosa | |
| Geographical availability | Assam, China North-Central, China South-Central, China Southeast, East Himalaya, Japan, Korea, Manchuria, Myanmar, Nepal, Taiwan, Tibet, Vietnam, West Himalaya | |
| Plant parts | Root | |
| Other cancers | Breast cancer | |
| Target gene or protein | ALDH1A1, Sox2, Oct4, Bax, Caspase 3, Bcl-2, STAT3 | |
| Gene or Protein evidence | EsA caused proliferation and mammosphere formation inhibition of breast CSCs, induced breast CSCs apoptotic death, suppressed the growth of tumors generated from breast CSCs significantly, the expressions of stemness proteins including ALDH1A1, Sox2, and Oct4 were downregulated, proapoptotic proteins, Bax and cleaved caspase-3 were upregulated, whereas the antiapoptotic protein Bcl-2 was reduced, IL-6/STAT3 pathway proteins including IL-6, phosphorylated STAT3 (Tyr705), and STAT3 (Ser727) were downregulated significantly in EsA-treated breast CSCs and tumor tissues. | |
| Target pathways | IL-6/STAT3 signaling pathway | |
| IC50 | EsA showed dose-dependent inhibitory effect on murine and human breast cancer cells and CSCs (p < 0.01). IC50 was 177.68 and 247.30 μg/ml for murine breast cancer cells and CSCs , respectively, 269.30 and 320.93 μg/ml for human breast cancer cells and CSCs , respectively. | |
| Potency | EsA inhibited breast CSC growth in vitro and in vivo through stemness attenuation and apoptosis induction by blocking IL-6/STAT3 signaling pathway, it might serve as a novel candidate agent for human breast cancer treatment and/or prevention. | |
| Cell line/ mice model | BALB/c mice, MCF-7 | |
| Additional information | EsA improved the clinical and pathological symptoms, inflammation and oxidative stress experienced by DNCB-induced mice and was involved in the inactivation of NLRP3 inflammasome by activating Nrf2. | |
| PubChem ID | 14132358 | |
| Additional PMIDs | 37439364 | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:676329-1 | |
| Safety | NA |