| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-2016 | |
| Phytochemical name or plant extracts | Berbamine | |
| PMID | 29445175 | |
| Literature evidence | Berbamine (BBM) is a natural compound extracted from traditional Chinese medicine that is widely used for treatment of a variety of diseases without any obvious side effects. | |
| IUPAC name | (1S,14R)-20,21,25-trimethoxy-15,30-dimethyl-7,23-dioxa-15,30-diazaheptacyclo[22.6.2.23,6.18,12.114,18.027,31.022,33]hexatriaconta-3(36),4,6(35),8,10,12(34),18,20,22(33),24,26,31-dodecaen-9-ol | |
| Phytochemicals’ class or type of plant extracts | Alkaloid | |
| Source of phytochemicals or plant Extracts | Berberis amurensis | |
| Geographical availability | Amur, China North-Central, China Southeast, Inner Mongolia, Japan, Khabarovsk, Korea, Manchuria, Mongolia, Primorye, Sakhalin | |
| Plant parts | NA | |
| Other cancers | Breast cancer | |
| Target gene or protein | SNAP29, VAMP8, BNIP3, VAMP8, Bcl-2, Bax, pro-MMP9/pro-MMP2, c-met , AKT, nuclear factor kappaB p-65, Bcl-2/Bax, osteopontin, VEGF, MMP9, MMP2 | |
| Gene or Protein evidence | Mechanistically, we found that BBM blocked autophagosome-lysosome fusion by inhibiting the interaction of SNAP29 and VAMP8. Furthermore, BBM induced upregulation of BNIP3 and the interaction between SNAP29 and BNIP3. BNIP3 depletion or SNAP29 overexpression abrogated BBM-mediated blockade of autophagosome-lysosome fusion through the interaction between SNAP29 and VAMP8, whereas BNIP3 overexpression blocked autophagosome-lysosome fusion through inhibition of the interaction between SNAP29 and VAMP8. BER down-regulates anti-apoptotic protein Bcl-2 levels and up-regulates pro-apoptotic protein Bax expressions in MDA-MB-231 and MDA-MB-435S cells. BER also has synergistic effects with anticancer agents trichostatin A, celecoxib and/or carmofur on reducing Bcl-2/Bax ratios and VEGF secretions in MDA-MB-231 cells. In addition, BER significantly suppresses cell migration and invasion, as well as decreases pro-MMP-9/pro-MMP-2 activation in breast cancer cells. Furthermore, BER suppresses Akt and nuclear factor kappaB signaling by reducing the phosphorylation of c-Met and Akt, and inhibiting their downstream targets such as nuclear factor kappaB p-65, Bcl-2/Bax, osteopontin, VEGF, MMP-9 and MMP-2 on protein and/or mRNA levels in breast cancer cells. | |
| Target pathways | Akt and NF-κB signaling | |
| IC50 | At 24, 48 and 72 h: 51.6 μM, 32.5 μM, 13.7 μM against MDA-MB-231 42.3 μM, 34.3 μM, and 25.0 μM against MDA-MB-435 | |
| Potency | These findings suggest that BER may have the wide therapeutic and/or adjuvant therapeutic application in the treatment of human breast cancer and other cancers. | |
| Cell line/ mice model | MDA-MB-231, MDA-MB-435S | |
| Additional information | BER shows synergistic effects with some existing anticancer agents such as trichostatin A (TSA, the histone deacetylase inhibitor), celecoxib (the inhibitor of COX-2), and carmofur against the growth of MDA-MB-231 cells. BER also displays the strong activity of inducing apoptosis in both estrogen receptor-negative MDA-MB-231 cells and estrogen receptor-alpha-positive MCF-7 breast cancer cells. | |
| PubChem ID | 275182 | |
| Additional PMIDs | 19796390 | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:106405-1 | |
| Safety | NA |