Properties |
Information |
PhytoCAT-ID |
PhytoCAT-539 |
Phytochemical name or plant extracts |
Aloe-emodin |
PMID |
33988779 |
Literature evidence |
The pharmacological actions of anthraquinones in cancer cells are known to induce apoptosis or autophagy, and revert multidrug resistance. |
IUPAC name |
1,8-dihydroxy-3-(hydroxymethyl)anthracene-9,10-dione |
Phytochemicals’ class or type of plant extracts |
Quinone |
Source of phytochemicals or plant Extracts |
Aloe vera |
|
Geographical availability |
Oman |
Plant parts |
NA |
Other cancers |
Breast cancer |
Target gene or protein |
Bcl-2, Bax, NF-κB, p38, ERK, miR-15a, miR-16-1, IL-1β, IL-6, VEGF, MMP2, MMP9 |
Gene or Protein evidence |
Mechanistically, AE dose-dependently decreased the protein expression of Bcl-2 and Bcl-xl, while it increased Bax protein expression in MCF-10AT and MCF-7 cells. Thus, our study demonstrated the effects of aloe-emodin and emodin-acid in controlling the migratory and invasive ability of 4T1 breast cancer cells, in addition to inhibiting NF-κB activity and the expression of its downstream target molecules. lthough aloe-emodin inhibited p38 and ERK phosphorylation.
Along with the mRNA expression, the enzymatic activities of MMP-2 and 9 in 4T1 cells were inhibited by both aloe-emodin and emodicacid in a dose-dependent manner
Both aloe-emodin and emodic-acid inhibited the secretion of the pro-tumorigenic cytokines IL-1β and IL-6, and VEGF and MMP expression, and subsequently inhibited the invasive and migratory potential of 4T1 cells.
In all candidate miRNAs that bind to 3'-UTR of Bcl-2, miR-15a and miR-16-1 were dose-dependently downregulated by AE. |
Target pathways |
Caspase-8 pathway |
IC50 |
35.75 μM for 72 h against MCF-10AT
43.49 μM 72 h against MCF-10AT |
Potency |
Moreover, inhibition of miR-15a/16-1 could eliminate the inhibition of MCF-10AT and MCF-7 cells growth by AE and could reverse the downregulation of AE-induced Bcl-2 protein level. |
Cell line/ mice model |
MCF-10A, MCF-10AT, MCF-7, MDA-MB-231, 4T1 |
Additional information |
Our research provides an important basis that AE induces BT cell apoptosis through upregulation of miR-15a/miR-16-1 that suppresses BCL2. |
PubChem ID |
10207 |
Additional PMIDs |
34124677 24577925 11459643 18563353 30600703 33988779 32190086 27703348 29783719 |
Additional sources of information |
https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:530017-1 |
Safety |
NA |