Properties |
Information |
PhytoCAT-ID |
PhytoCAT-52 |
Phytochemical name or plant extracts |
Cimicifuga racemosa extract |
PMID |
12408370 |
Literature evidence |
To determine the influence of one such alternative, black cohosh (Cimicifuga racemosa [CR]), on estrogen-dependent mammary cancers, we conducted an in vitro investigation of the effect of an isopropanolic CR-extract on the proliferation of estrogen receptor-positive breast cancer cells. |
IUPAC name |
NA |
Phytochemicals’ class or type of plant extracts |
Isopropanolic extract |
Source of phytochemicals or plant Extracts |
Cimicifuga racemosa |
|
Geographical availability |
Alabama, Arkansas, Connecticut, Delaware, District of Columbia, Georgia, Illinois, Indiana, Kentucky, Maryland, Massachusetts, Missouri, New Jersey, New York, North Carolina, Ohio, Ontario, Pennsylvania, South Carolina, Tennessee, Virginia, West Virginia |
Plant parts |
NA |
Other cancers |
Breast cancer |
Target gene or protein |
Caspases, ER, p21, Cyclin D1, Progesterone receptor B1 |
Gene or Protein evidence |
In addition, the involvement of activated caspases was supported by the cleavage of cytokeratin 18 detected with M30 antibody. Increases in the level of M30-antigen of about 4-fold and 2-fold over untreated controls were observed in C. racemosa -treated MCF-7 and MDA-MB231 cells.
These results suggested that C-Ex does not activate or inactivate ERalpha in a direct manner, but the extracts may affect factors in ER signal transduction pathway.
Also, we evaluated the effects of this CR extract on the transcriptional regulation of genes involved in cell cycle progression in the ER-negative cell lines 293T and T-47D and we found that this extract markedly inhibited the luciferase activity driven by the cyclin D1 promoter and increased the transcriptional activity of the p21 gene promoter.
Finally, we observed that our CR extract bound to the progesterone receptor B1 but did not show progestin-like activity in the T-47D cell line. |
Target pathways |
ER signal transduction pathway |
IC50 |
Down regulation of the proliferative activity and cell killing by isopropanolic and ethanolic extracts occurred in a clear dose-dependent response with a 50% growth inhibitory concentration of 54.1 +/- 11.4 and 80.6 +/- 17.7 micro g/ml in MCF-7 cells and of 29.5 +/- 3.0 and 58.6 +/- 12.6 microg/ml in MDA-MB231 cells, respectively. |
Potency |
Under estrogen-deprived conditions, the CR-extract (10(-3)-10(-5) dilutions) significantly inhibited MCF-7 cell proliferation.
Results showed that iCR was not associated with an increase in the risk of recurrence but associated with prolonged disease-free survival.
Additionally, application of the CR-extract inhibited estrogen-induced proliferation of MCF-7 cells.
In conclusion, with its positive benefit-risk profile, iCR/iCR + HP may offer a safe non-hormonal therapeutic option for breast cancer survivors receiving endocrine therapy. |
Cell line/ mice model |
MCF-7, MDA-MB-231, T47D, LNCaP |
Additional information |
These results indicate that C.
racemosa extract exerts no proliferative activity, but kills the estrogen receptor positive MCF-7 as well as estrogen receptor negative MDA-MB231 cells by activation of caspases and induction of apoptosis.
Such data that suggest a non-estrogenic, or estrogen-antagonistic effect of CR on human breast cancer cells lead to the conclusion that CR treatment may be a safe, natural remedy for menopausal symptoms in breast cancer.
A significant reduction of cell growth was observed at a concentration as low as 50 ng/ml.
Thus, it is demonstrated for the first time that CR compounds potently inhibit the growth of human prostate cancer cells in vitro.
This anti-proliferative effect may be mediated via the AhR.
Finally, we observed that our CR extract bound to the progesterone receptor B1 but did not show progestin-like activity in the T-47D cell line.
These findings provide new mechanistic insights into the antiproliferative activities of CR in ER-positive and ER-negative tumour cell lines and highlight their potential in the management of climacteric disorders in women with a history of breast cancer. |
PubChem ID |
NA |
Additional PMIDs |
12609558 14999145 15830838 15577215 16557472 17416109 23210246 23972793 25713759 30626212 12058323 |
Additional sources of information |
https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:1210182-2 |
Safety |
NA |