AKT1 and colorectal cancer: Akt phosphorylation was down-regulated and NF-κB p65 activation was suppressed in TESC siRNA-expressing colorectal cancer cells (Fig. 4C, F), indicating that TESC might increase the survival of colorectal cancer cells through the Akt-dependent NF-κB pathway, but not JNK, ERK1/2, and p38 MAPK signaling pathways.