Supplementary Tables and Figures from AKT1 Inhibits Epithelial-to-Mesenchymal Transition in Breast Cancer through Phosphorylation-Dependent Twist1 Degradation

Supplementary Table S1. Relationship between expression of AKT1, β-TrCP, Twist1, and E-cadherin in surgical specimens of breast cancer. Supplementary Table S2. Antibodies used in Western blotting and immunoprecipitation. Supplementary Figure S1. AKT1 is downregulated in aggressive breast cancer. Supplementary Figure S2. AKT1 preferentially interacts with Twist1. Supplementary Figure S3. AKT1 phosphorylates Twist1 at two putative motifs. Supplementary Figure S4. AKT1 induces β-TrCP mediated Twist1 degradation. Supplementary Figure S5. Twist1 AVA induces a stronger EMT phenotypic change. Supplementary Figure S6. Twist1 AVA induces a stronger EMT phenotypic change. Supplementary Figure S7. Clinical association of AKT1, β-TrCP, Twist1 and E-caherin expression in breast cancer patients. Supplementary Figure S8. MK-2206 induces EMT phenotypic change. Supplementary Figure S8. Clinical association of AKT1, β-TrCP, Twist1 and E-caherin expression in breast cancer patients. Supplementary Figure S9. MK-2206 induces EMT phenotypic change.