Knockdown of DEAD-box 51 inhibits tumor growth of esophageal squamous cell carcinoma via the PI3K/AKT pathway

Figure 4 Knockdown of DEAD-box helicase 51 induced inactivation of the phosphoinositide 3-kinase/AKT signaling pathway. A-E: Expression of phosphoinositide 3-kinase (PI3K)/AKT pathway members, including phosphatase and tenin homolog (PTEN), phosphorylated PTEN (p-PTEN), PI3K, p-PI3K, AKT, p-AKT, mammalian target of rapamycin (mTOR) and p-mTOR, was detected by western blot analysis; F: AKT activator insulin-like growth factor 1 (IGF-1) reversed the inhibitory effect of DDX51 knockdown on the proliferation of TE-1 cells; G: AKT activator IGF-1 reversed the pro-apoptotic effect of DDX51 knockdown on the proliferation of TE-1 cells. ^aP < 0.05. All data were obtained from at least three independent experiments. Negative control was a scrambled small interfering RNA.