| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-1483 | |
| Phytochemical name or plant extracts | Antrodin C | |
| PMID | 25658913 | |
| Literature evidence | The inhibition of MMPs and uPA activity by ADC was reasoned by suppression of its corresponding transcription factor β-catenin. | |
| IUPAC name | 3-Isobutyl-4-[4-(methyl-2-butenyloxy)phenyl]-1H-pyrrole-2,5-dione | |
| Phytochemicals’ class or type of plant extracts | Pyrrolidione | |
| Source of phytochemicals or plant Extracts | Antrodia cinnamomea | |
| Geographical availability | Taiwan | |
| Plant parts | Mycelia | |
| Other cancers | Breast cancer | |
| Target gene or protein | E-cadherin, occludin, N-cadherin, Vimentin, MMP2, MMP9 | |
| Gene or Protein evidence | Pretreatment of MCF-7 cells with ADC significantly blocked TGF-β1-induced phenotypic changes and actin cytoskeleton remodeling. In addition, ADC was able to up-regulate epithelial markers such as E-cadherin and occludin, whereas mesenchymal markers including N-cadherin and vimentin were significantly inhibited, possibly through the modulation of transcriptional regulators Smad/Smad3. ADC blocked TGF-β1-induced migration and invasion of MCF-7 cells through the down-regulation of matrix-metalloproteinases (MMP-2, -9) | |
| Target pathways | Taken together, our data suggested that ADC attenuates the TGF-β1-induced EMT, migration and invasion of human breast carcinoma through the suppression of Smad2/3 and β-catenin signaling pathways. | |
| IC50 | NA | |
| Potency | NA | |
| Cell line/ mice model | MCF-7 | |
| Additional information | ADC blocked TGF-β1-induced migration and invasion of MCF-7 cells through the down-regulation of matrix-metalloproteinases (MMP-2, -9) and urokinase plasminogen activator (uPA). The inhibition of MMPs and uPA activity by ADC was reasoned by suppression of its corresponding transcription factor β-catenin. | |
| PubChem ID | NA | |
| Additional PMIDs | NA | |
| Additional sources of information | NA | |
| Safety | NA |