Table 3.
Recent studies on drugs or chemical substances that suppress EMT-induced cancer stem-like cell initiation
| Drugs or chemical substances | Cancers | Mechanisms | References |
|---|---|---|---|
| Honokiol | Renal cancer | Modulates miR-141/ZEB2 signaling | 127 |
| DFOG | Gastric cancer | Downregulation of FoxM1 and Twist1 expression | 128 |
| EGFR inhibitors such as erlotinib and cetuximab | Esophageal squamous-cell carcinoma | Suppression of TGF-β and ZEB1-mediated EMT and activation of Notch1 and Notch3 to induce tumor cell differentiation | 129 |
| Silibinin | Bladder cancer | Inactivation of β-catenin/ZEB1 signaling | 130 |
| γ-Secretase inhibitor IX | Pancreatic ductal adenocarcinoma | Inhibition of the Notch signaling pathway that induces EMT and suppression of the growth of CD44+/EpCAM+ cells | 131 |
| Valproic acid | Esophageal squamous-cell carcinoma | Unclear | 132 |
| Pomegranate extract P123 | Breast cancer | Downregulates genes such as TWIST1 involved in EMT as an agonist of BMP signaling, blocking TGF-β | 133 and 134 |
| Dioscin | Melanoma | Polarizes macrophages toward the M1 phenotype | 135 |
Abbreviations: EMT, epithelial–mesenchymal transition; DFOG, 7-difluoromethoxyl-5,4′-di-n-octyl genistein; EGFR, epidermal growth factor receptor; FoxM1, forkhead box M1; TGF, transforming growth factor; BMP, bone morphogenetic protein.