Properties |
Information |
PhytoCAT-ID |
PhytoCAT-566 |
Phytochemical name or plant extracts |
Delphinidin |
PMID |
18499206 |
Literature evidence |
Delphinidin, present in pigmented fruits and vegetables possesses potent anti-oxidant, anti-inflammatory and anti-angiogenic properties. |
IUPAC name |
2-(3,4,5-trihydroxyphenyl)chromenylium-3,5,7-triol,chloride |
Phytochemicals’ class or type of plant extracts |
Flavonoid |
Source of phytochemicals or plant Extracts |
Punica granatum |
|
Geographical availability |
Afghanistan, Iran, Iraq, North Caucasus, Pakistan, Tadzhikistan, Transcaucasus, Turkey, Turkmenistan |
Plant parts |
Fruits |
Other cancers |
Breast cancer, Lung cancer |
Target gene or protein |
Cyclin B1, CDK-1, NF-κB, NF-κB/p65, PKCalpha, IKKalpha/beta, IkappaBalpha, STAT-3, MMP9, HER2, PARP, Caspase 3, Bcl-2, BAX, EGFR, AKT, MAPK, PI3K |
Gene or Protein evidence |
In the present study, it was found that delphinidin could induce G2/M phase cell cycle arrest by inhibiting the protein expression level of cyclin B1 and Cdk1 in HER-2-positive breast cancer cell lines.
Delphinidin was found to repress HGF-activated NFkappaB transcription with a decrease in (i) phosphorylation of IKKalpha/beta and IkappaBalpha, and (ii) activation and nuclear translocation of NFkappaB/p65.
Inhibition of HGF-mediated membrane translocation of PKCalpha as well as decreased phosphorylation of STAT3 was further observed in delphinidin treated cells.
Delphinidin significantly suppressed PMA-induced MMP-9 protein expression in MCF-7 human breast carcinoma cells, and it also inhibited the MMP-9 gene transcriptional activity by blocking the activation of NFkappaB (NF-κB) through MAPK signaling pathways.
Recent drug discovery efforts have demonstrated that naturally occurring polyphenolic compounds like delphinidin have potential to inhibit proliferation and promote apoptosis of breast cancer cells by targeting HER2 receptors.
Further, delphinidin treatment of AU-565 cells inhibited EGF-induced autophosphorylation of EGFR, AKT and MAPK, activation of PI3K and cell invasion.
We then compared the growth inhibitory effects of delphinidin (5-40 microM; 48 hr), and found that it resulted in a decrease in cell growth of AU-565 and MCF-10A cells but had only minimal effects on normal mammary epithelial 184A1 cells.
Treatment of AU-565 cells with delphinidin resulted in (i) induction of apoptosis, (ii) cleavage of PARP protein, (iii) activation of caspase-3 and (iv) downregulation of Bcl-2 with an increase in the expression of Bax. |
Target pathways |
NF-κB and MAPK signaling pathway
ERK and NF-κB signaling pathway
JNK signaling pathway
Ras-ERK MAPKs pathway
PI3K/AKT/mTOR/p70S6K pathway |
IC50 |
41.42 µM against MDA-MB-453
60.92 µM against BT-474 |
Potency |
In addition, delphinidin was found to be a potent inhibitor of epidermal growth factor receptor (EGFR) and its downstream signaling pathways in AU-565 breast cancer cells (Zaman et al., 2006).
Overall, the findings from the present study demonstrated that delphinidin treatment could induce the mitochondrial apoptosis pathway in human HER-2-positive breast cancer cell lines, providing an experimental basis for the prevention and treatment of HER-2-positive breast cancer by flavonoids. |
Cell line/ mice model |
MDA-MB-453, AU-565, MCF-10A, MCF-7, BT-474 |
Additional information |
Delphinidin-mediated inactivation of PKCα may be responsible for reduced cell proliferation and neoplastic transformation of HGF-treated cells.
|
PubChem ID |
68245 |
Additional PMIDs |
34854367 21792311 18623129 23975834 25000305 18499206 34712357 27221932 |
Additional sources of information |
https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:554129-1 |
Safety |
NA |