Figure 7

Crosstalk between PI3K-Akt and NFκB pathways after BTG2 expression in normal and cancer cells via activation of Akt1 and degradation of IκBα protein. The endogenous and exogenous expressions of BTG2^/TIS21 significantly induces IκBα degradation via Atk1 activation in cancer and normal cells. The activated NFκB (p65) binds to the enhancer element on the 2^nd intron, not promoter, of MnSOD gene and upregulates its transcription in response to BTG2^/TIS21 expression. The induction of MnSOD expression triggers scavenge of ROS level and the BTG2-mediated ROS reduction inhibits cell cycle progression at G2 phase entry via inhibition of cyclin B1 biosynthesis in contrast to the upregulation of p21^WAF1 expression.