| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-1183 | |
| Phytochemical name or plant extracts | Baicalin | |
| PMID | 15586243 | |
| Literature evidence | All four compounds inhibited MCF-7 and T-47D cell proliferation, baicalin being the most potent inhibitor. | |
| IUPAC name | (2S,3S,4S,5R,6S)-6-(5,6-dihydroxy-4-oxo-2-phenylchromen-7-yl)oxy-3,4,5-trihydroxyoxane-2-carboxylic acid | |
| Phytochemicals’ class or type of plant extracts | Flavonoid | |
| Source of phytochemicals or plant Extracts | Scutellaria baicalensis | |
| Geographical availability | Amur, Buryatiya, China North-Central, China South-Central, Chita, Inner Mongolia, Irkutsk, Khabarovsk, Korea, Manchuria, Mongolia, Primorye, Vietnam, Yakutskiya | |
| Plant parts | Root | |
| Other cancers | Breast cancer | |
| Target gene or protein | miR-338-3p, MORC4, ALPP, DUSP1, CYR61, ALPPL2, SPP1, TLR4, EMT | |
| Gene or Protein evidence | In conclusion, baicalin suppressed cell viability, migration and invasion but promoted apoptosis in BC cells by regulating miR-338-3p and MORC4, indicating the promising pharmacological value of baicalin in BC treatment. Based on the transcriptome sequencing of the bone metastases group and the baicalin treatment group, baicalin inhibited the expression of ALPP, DUSP1, CYR61, ALPPL2, SPP1 and TLR4. Taken together, these results suggest that baicalin and baicalein of Scutellaria baicalensis Georgi may suppress the EMT of breast epithelial cells and the tumorigenic activity of breast cancer cells. | |
| Target pathways | Baicalin inhibits the metastasis of highly aggressive breast cancer cells by reversing epithelial-to-mesenchymal transition by targeting β-catenin signaling.. These findings suggested that baicalein, acting as a prooxidant, could trigger apoptosis in MCF-7 cells occurs via the ROS-mediated intrinsic mitochondria-dependent pathway. | |
| IC50 | 57.41 ± 1.15 μM against MCF-7 | |
| Potency | We found that baicalin had the potential to suppress the migration and invasion of highly aggressive breast cancer cells in a dose-dependent manner but had no impact on the viability of these cancer cells. | |
| Cell line/ mice model | T-47D, MCF-7, MDA-MB-231 | |
| Additional information | Taken together, all these results indicate that baicalin effectively suppresses the metastasis of breast cancer by reversing EMT, which may be mediated by downregulation of β-catentin expression.. The findings of this study demonstrate that the effect of baicalin on Dox treatment could enhance cytotoxicity toward breast cancer cells via the ROS/[Ca2+]i-mediated intrinsic apoptosis pathway-thus potentially lessening the required dosage of doxorubicin, and further exploring associated mechanisms in combined treatments for breast cancer clinical interventions in the future. | |
| PubChem ID | 64982 | |
| Additional PMIDs | 15586243 11746275 25686495 34815689 34295892 31908485 34330116 34679641 29039569 26578185 12208892 19836937 24026776 31849483 | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:458155-1 | |
| Safety | Further analysis revealed that baicalin and baicalein, the major flavones of these butanol extracts, inhibited TGF-β1-mediated EMT by reducing the expression level of the EMT-related transcription factor, Slug via the NF-κB pathway, and subsequently increased migration in MCF10A cells. |