| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-1034 | |
| Phytochemical name or plant extracts | Caesalpinia spinosa extract (P2Et) | |
| PMID | 27253407 | |
| Literature evidence | Moreover, the tumor protective effects of P2Et treatment were abolished in immunodeficient mice, and partially lost after CD4 and CD8 depletion, indicating that P2Et's anti-tumor activity is highly dependent on immune system and at least in part of T cells. | |
| IUPAC name | NA | |
| Phytochemicals’ class or type of plant extracts | Polyphenol rich extract | |
| Source of phytochemicals or plant Extracts | Caesalpinia spinosa | |
| Geographical availability | Bolivia, Chile Central, Chile North, Colombia, Cuba, Ecuador, Peru, Venezuela | |
| Plant parts | NA | |
| Other cancers | Breast cancer, Skin cancer | |
| Target gene or protein | Caspase 3, Caspase 9, CD4, CD8, Calreticulin , IFN-γ | |
| Gene or Protein evidence | P2Et treatment results in activation of caspase 3 and 9, mobilization of cytochrome c and externalization of annexin V in tumor cells, thus suggesting the induction of apoptosis. Moreover, the tumor protective effects of P2Et treatment were abolished in immunodeficient mice, and partially lost after CD4 and CD8 depletion, indicating that P2Et's anti-tumor activity is highly dependent on immune system and at least in part of T cells. We show that P2Et extract and ethyl gallate induced autophagy, partially protecting tumor cells from death and promoting calreticulin exposure and the release of ATP. We further demonstrate that P2Et-treated tumor cells are highly immunogenic in vaccinated mice and induce immune system activation, clearly shown by the generation of interferon gamma (IFN-γ) producing tyrosine-related protein 2 antigen-specific CD8+ T cells. | |
| Target pathways | NA | |
| IC50 | NA | |
| Potency | NA | |
| Cell line/ mice model | B16F10, A375, 4T1 | |
| Additional information | Furthermore, P2Et can decrease the factors involved in tissue damage by reducing IL-6 and decrease ILC2 cells of the lung in animals with lung metastases. Here, we show that inducing autophagic flux with P2Et protects cancer cells from cell death and that this delay in cell death is required for the generation of immunogenic signals. This study shows that combined therapy of P2Et and anti-PD-L1 can improve antitumor response in a melanoma model by activating the immune response and neutralizing immunosuppressive mechanisms. | |
| PubChem ID | NA | |
| Additional PMIDs | 33156457 33312174 | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:40114-2 | |
| Safety | NA |