| Properties | Information1 | Information2 |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-1612 | PhytoCAT-1886 |
| Phytochemical name or plant extracts | Clinacanthus nutans extract (CN) | Clinacanthus nutans extract (CN) |
| PMID | 34379689 | |
| Literature evidence | Overall, CN acts by ameliorating the pro-inflammatory condition in the TME and may be a potential strategy for its anticancer mechanism on highly metastatic breast cancer condition. | However, only ethyl acetate extract caused the loss of mitochondrial membrane potential. |
| IUPAC name | NA | NA |
| Phytochemicals’ class or type of plant extracts | Extract | Methanolic extract, ethyl acetate extract |
| Source of phytochemicals or plant Extracts | Clinacanthus nutans | Clinacanthus nutansindau |
| Geographical availability | Borneo, Cambodia, China South-Central, China Southeast, Hainan, Jawa, Laos, Lesser Sunda Is., Malaya, Thailand, Vietnam | Borneo, Cambodia, China South-Central, China Southeast, Hainan, Jawa, Laos, Lesser Sunda Is., Malaya, Thailand, Vietnam |
| Plant parts | Leaves | Root |
| Other cancers | Breast cancer | Breast cancer, Cervical cancer |
| Target gene or protein | IL-6, IL-1β, TNF-α. | Bcl-2 |
| Gene or Protein evidence | CN extracts prevented the smoldering inflammation between cancer cells and immune cells by reducing the level of pro-inflammatory cytokines, such as IL-6, IL-1β and TNF-α. | Although both root extracts exhibited apoptotic effect based on morphological changes and the suppression of BCL2 expression. |
| Target pathways | LPS-induced production of pro-inflammatory cytokines were regulated by multiple pathways such as Nrf2/Keap1 and NF-κB pathways thus overlapping modulation of these pathways may have occurred at certain CN concentration as previously shown by other plant phytochemicals | NA |
| IC50 | NA | Methanolic extract - 35 μg/mL against MCF-7 Ethyl acetate extract - 30 μg/mL against MCF-7 |
| Potency | CN was not cytotoxic to both MDA-MB-231 and THP-1 cells. The ability of MDA-MB-231 to migrate was also not halted by CN treatment. | he results demonstrated that root extracts promote apoptosis by suppressing BCL2 via mitochondria-dependent or independent manner. The identified compounds might work solely or cooperatively in regulating apoptosis. |
| Cell line/ mice model | MDA-MB-231 | MCF-7, HTB-22, HeLa, CCL-2, NIH 3T3, CRL-1658 |
| Additional information | TNF-α were significantly decreased after CN ethanol treatment at concentration 25- (p = 0.001), 50- (p = 0.000) and 100 μg/mL (p = 0.000). CN aqueous extract slightly inhibited TNF-α at all 25-50- and 100 μg/mL (p = 0.001, p = 0.000, p = 0.000, respectively). Overall, CN acts by ameliorating the pro-inflammatory condition in the TME and may be a potential strategy for its anticancer mechanism on highly metastatic breast cancer condition. The major pathways that link both cancer and inflammation were NF-κB and STATs thus further study on the upstream and downstream pathways is needed to fully understand the mechanism of CN extracts in cooling the inflamed TME in breast cancer. | NA |
| PubChem ID | NA | |
| Additional PMIDs | NA | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:46937-1 | |
| Safety | NA | NA |