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. 2015 Oct 20;6(41):43540–43556. doi: 10.18632/oncotarget.6183

Figure 3. AKT is an upstream regulator of SOX2 protein expression.

Figure 3

(A) Dose-dependent co-depletion of pAKT and SOX2 proteins following MK-2206 treatment in BC cell lines (MCF7, BT474, T47D) and patient-derived cells (P1, P2) within 48 hours of incubation. Note the grossly unaltered levels of total AKT. Anti-actin staining is shown for reference. (B) Temporal resolution of pAKT and SOX2 protein expression in MCF7 cells upon AKT inhibition throughout an observation window of 24 hours. (C) Transfection with myristoylated AKT1 induces both pAKT and SOX2 protein expression in MCF7 cells. (D) Confirmation of SOX2 protein depletion by the alternative AKT kinase inhibitor Akti1/2 and upstream PI3K inhibitors (wortmannin and GCD-0941) in MCF7 cells. AKT downstream inhibitor rapamycin has no impact on SOX2 expression, instead. Functional integrity of reagents was verified by uniform depletion of pRPS6. Mock-treated control lanes are shown at the left. (E) Schematic illustration of the canonical PI3K/AKT/TORC1 pathway. Green: drugs that impair SOX2 protein expression.