| Properties | Information |
|---|---|
| PhytoCAT-ID | PhytoCAT-1587 |
| Phytochemical name or plant extracts | Cotylenin A |
| PMID | 18754885 |
| Literature evidence | Taken together, our results suggest that cotylenin A and rapamycin induce inhibition of cancer cell growth through the induction of cyclin G2. |
| IUPAC name | (1R,2E,4R,7S,8R,9R,10R)-10-[[(1R,4S,9S)-5-hydroxy-2-(methoxymethyl)-9-methyl-9-(oxiran-2-yl)-3,7,10,11-tetraoxatricyclo[6.2.1.01,6]undecan-4-yl]oxy]-4-(methoxymethyl)-1,8-dimethyl-12-propan-2-yltricyclo[9.3.0.03,7]tetradeca-2,11-diene-4,9-diol |
| Phytochemicals’ class or type of plant extracts | Plant growth regulator |
| Source of phytochemicals or plant Extracts | NA |
| Geographical availability | NA |
| Plant parts | NA |
| Other cancers | Breast cancer |
| Target gene or protein | Cyclin G2, AKT, mTOR |
| Gene or Protein evidence | cotylenin A and rapamycin rapidly and markedly induced the cyclin G2 gene expression in several cancer cells including MCF-7 cells. In this study, we found that cotylenin A could suppress rapamycin-induced phosphorylation of Akt (Ser473) in MCF-7 cells and lung carcinoma A549 cells and that cotylenin A also enhanced the rapamycin-induced growth inhibition of MCF-7 and A549 cells. Cotylenin A, a plant growth regulator, and rapamycin, an inhibitor of mammalian target of rapamycin (mTOR), are potent inducers of differentiation of myeloid leukemia cells. |
| Target pathways | NA |
| IC50 | NA |
| Potency | Recently, we found that cotylenin A and rapamycin effectively inhibited the proliferation of several human breast cancer cell lines including MCF-7. |
| Cell line/ mice model | MCF-7 and A549 |
| Additional information | The growth arrest of the MCF-7 cells at the G1 phase, induced by the treatment with cotylenin A and rapamycin or the culture in low serum medium, markedly induced the cyclin G2 gene expression. Furthermore, cyclin G2 knockdown induced by cyclin G2 small interfering RNA markedly reduced the potency of cotylenin A plus rapamycin to induce growth inhibition. Taken together, our results suggest that cotylenin A and rapamycin induce inhibition of cancer cell growth through the induction of cyclin G2. Inhibition of rapamycin-induced Akt phosphorylation by cotylenin A correlates with their synergistic growth inhibition of cancer cells. However, the mechanisms of the combined effects of cotylenin A and rapamycin are still unknown. In this study, we found that cotylenin A could suppress rapamycin-induced phosphorylation of Akt (Ser473) in MCF-7 cells and lung carcinoma A549 cells and that cotylenin A also enhanced the rapamycin-induced growth inhibition of MCF-7 and A549 cells. These results suggest that the inhibition of rapamycin-induced Akt phosphorylation by cotylenin A correlates with their effective growth inhibition of cancer cells. |
| PubChem ID | 5458687 |
| Additional PMIDs | 23255002 |
| Additional sources of information | NA |
| Safety | NA |