| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-1172 | |
| Phytochemical name or plant extracts | Emodin | |
| PMID | 32735937 | |
| Literature evidence | Besides, decreased p-FAK expression or regression in Mammosphere & tumor size in ex-ovo xenograft model is indicative of the better anti-tumorigenic potential of the dual formulation. | |
| IUPAC name | 1,3,8-trihydroxy-6-methylanthracene-9,10-dione | |
| Phytochemicals’ class or type of plant extracts | Quinone | |
| Source of phytochemicals or plant Extracts | Rheum palmatum | |
| Geographical availability | China North-Central, China South-Central, Inner Mongolia, Qinghai, Tibet, Vietnam | |
| Plant parts | NA | |
| Other cancers | Breast cancer | |
| Target gene or protein | IRF4, STAT6, Runx2, Bcl-2, Bax, Cytochrome c, MMP9, activator -1, NF-κB, miR-34a, IRF4, EMT | |
| Gene or Protein evidence | Emodin inhibited IRF4, STAT6, and C/EBPβ signaling and increased inhibitory histone H3 lysine 27 tri-methylation (H3K27m3) on the promoters of M2-related genes in tumor-associated macrophages. The Quinone derivative Emodin inhibits angiogenesis and metastasis through downregulating Runx2 activity in breast cancer. The results of the study further showed that Bcl-2 level decreased, while Bax and cytosolic cytochrome c levels in sample cells increased after the emodin treatment by using Western blot. Taken together, these results suggest that emodin inhibits the invasiveness of human cancer cells by suppressing MMP-9 expression through inhibiting AP-1 and NF-kappaB signaling pathways. Inhibitory effect of emodin on tumor invasion through suppression of activator protein-1 and nuclear factor-kappaB. Moreover, we demonstrate that miR-34a is upregulated by curcumin and emodin. Emodin suppressed the phosphorylation of two mitogen-activated protein kinases, extracellular signal-regulated protein kinase and c-Jun N-terminal kinase, but not p38 kinase, leading to reduced c-Jun phosphorylation and AP-1 DNA-binding. Natural compound emodin suppresses EMT and CSC formation of breast cancer cells by blocking TGF-β1-mediated crosstalk between TAMs and breast cancer cells. | |
| Target pathways | C/EBPβ signalling AP-1 and NF-κB signaling pathways | |
| IC50 | 37.57 μM against MCF-7 | |
| Potency | It was revealed here that EMD attenuated tumor cell-induced metastasis and angiogenesis both in vitro and in vivo. Furthermore, it was found that these inhibitory effects were caused by MMPs and VEGFR-2 inhibition in metastatic breast cancer cells and endothelial cells, respectively. | |
| Cell line/ mice model | MCF-7, 4T1, ZR-75-1, MDA-MB-453, MDA-MB-231, mice bearing EO771 or 4T1 | |
| Additional information | In addition, emodin inhibited tumor cell secretion of MCP1 and CSF1, as well as expression of surface anchoring molecule Thy-1, thus suppressing macrophage migration toward and adhesion to tumor cells. In this study, we report for the first time that combined curcumin and emodin administration synergistically inhibits proliferation (MTT assay), survival (flow cytometry), and invasion (transwell migration assay) of breast cancer cells. | |
| PubChem ID | 3220 | |
| Additional PMIDs | 22982073 23768005 24577925 11459643 14693052 18566240 25673059 32735937 32724475 33542691 27196773 23771315 23669265 15194008 23106482 23661994 30648710 34124677 30449167 18563353 25226568 14644660 26815015 31462111 27998305 18563356 | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:696772-1 | |
| Safety | NA |