Supplementary Data from Mcl-1 Interacts with Akt to Promote Lung Cancer Progression

Supplementary Figure 1. Knockout of Mcl-1 from H1299 by CRISPR/Cas9 system results in decreased cell proliferation and increased caspase 3/7 activity. Supplementary Figure 2. Expression of constitutive active form of Akt in H1299 Mcl-1 knockout cells restores cell growth. Supplementary Figure 3. Depletion of Mcl-1 by shRNA retards the growth of H460 lung xenografts. Supplementary Figure 4. Expression of WT Mcl-1 but not the PEST deletion mutant Mcl-1 in H1299 Mcl-1 knockout cells restores Akt/PDK1 and Akt/mTORC2 interactions. Supplementary Figure 5. Treatment of H1299 cells with PH-687 results in increased intramolecular PH/KD interactions in Akt and decreased interaction of Akt with PDK1 or mTORC2. Supplementary Figure 6. Mcl-1/Akt signaling pathway is essential for PH-687 inhibition of cancer cell growth. Supplementary Figure 7. Knockout of Mcl-1 or treatment of cells with PH-687 inhibits growth factor (s)-stimulated Akt activation. Supplementary Figure 8. In vivo toxicity analysis. Supplementary Methods