FIGURE 7

Molecular mechanisms for overexpression of SELENBP1 inhibiting the malignant progression and inducing the apoptosis in NSCLC cells. Overexpression of SELENBP1 decreased the expression of PI3K, p‐PI3K, AKT, p‐AKT, mTOR, p‐mTOR, and Bcl‐2, whereas increased the expression of Bax and caspase‐3. Overexpression of SELENBP1 suppressed the malignant progression of NSCLC cells by inhibiting the PI3K/AKT/mTOR signaling. Moreover, overexpression of SELENBP1 inducing the apoptosis of NSCLC cells was associated with the activation of caspase‐3‐dependent axis under nonhigh level of oxidative stress. Furthermore, overexpression of SELENBP1 facilitating the cell apoptosis under high level of oxidative stress was related to its combining with GPX1 and colocalizing in nucleus (ROS, reactive oxygen species).