| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-1723 | |
| Phytochemical name or plant extracts | Elephantopus mollis Kunth extract | |
| PMID | 32763415 | |
| Literature evidence | Elephantopus mollis Kunth extracts induce antiproliferation and apoptosis in human lung cancer and myeloid leukemia cells. | |
| IUPAC name | NA | |
| Phytochemicals’ class or type of plant extracts | Methanolic extract, ethyl acetate extract | |
| Source of phytochemicals or plant Extracts | Elephantopus mollis Kunth | |
| Geographical availability | Argentina Northeast, Argentina Northwest, Belize, Bolivia, Brazil North, Brazil Northeast, Brazil South, Brazil Southeast, Brazil West-Central, Colombia, Costa Rica, Cuba, Dominican Republic, Ecuador, El Salvador, French Guiana, Guatemala, Guyana, Haiti, Honduras, Jamaica, Leeward Is., Mexico Central, Mexico Gulf, Mexico Northeast, Mexico Northwest, Mexico Southeast, Mexico Southwest, Nicaragua, Panamá, Paraguay, Peru, Puerto Rico, Suriname, Trinidad-Tobago, Uruguay, Venezuela, Windward Is. | |
| Plant parts | Whole-plant | |
| Other cancers | Breast cancer, Colorectal cancer, Lung cancer | |
| Target gene or protein | PCNA, Bid, Bak, Bcl-2, p53 | |
| Gene or Protein evidence | Furthermore, mechanisms of EM extracts were elucidated. The significant downregulation of PCNA mRNA level induced by EM-EA/PE extracts contributed to the cell-growth restraint. EM-EA extract might activate apoptosis in A549 cells through both extrinsic and intrinsic signaling pathways by causing a 1.55-fold increase in BID, 3.65-fold increase in BAK and 3.11-fold decrease in BCL-2 expression level. Meanwhile, with EM-EA-extract treatment, HL60 cells might encounter P53-dependent apoptotic deaths. | |
| Target pathways | NA | |
| IC50 | Methanolic extract - 3.97 μg/mlagainst MCF-7 Ethyl acetate extract - 12.57 μg/ml against T47D | |
| Potency | The combination of antiproliferation and apoptosis activation contributed to the high efficacy of EM extracts. These findings not only proved the anticancer potential of EM but also provided further insights into the mechanisms of EM extracts. | |
| Cell line/ mice model | MCF-7, A549, T47D, HepG2, DLD-1, NCI-H23 | |
| Additional information | The significant downregulation of PCNA mRNA level induced by EM-EA/PE extracts contributed to the cell-growth restraint. EM-EA extract might activate apoptosis in A549 cells through both extrinsic and intrinsic signaling pathways by causing a 1.55-fold increase in BID, 3.65-fold increase in BAK and 3.11-fold decrease in BCL-2 expression level. Meanwhile, with EM-EA-extract treatment, HL60 cells might encounter P53-dependent apoptotic deaths. | |
| PubChem ID | NA | |
| Additional PMIDs | NA | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:202942-1 | |
| Safety | NA |