The results revealed that resveratrol treatment and AKT1 knockdown significantly inhibited cell migration and invasion in colon cancer, and markedly increased E‑cadherin expression and decreased that of N‑cadherin, phospho (p)‑AKT1, p‑GSK‑3β, and Snail in colon cancer both in vitro and in vivo.
The results have shown that 3,5-diamino-N-[3-(trifluoromethyl)phenyl]benzamide (4d) exhibited significant tumor cytotoxicity against human colon cancer cells (HCT-116) with IC<sub>50</sub> of 8.3 μm and showed commendable selectivity to GSK-3β.
In this study, we found that idelalisib treatment induces PUMA in colon cancer cells irrespective of p53 status through the p65 pathway following AKT inhibition and glycogen synthase kinase 3β (GSK3β) activation.
Celecoxib and etoricoxib, the two cyclooxygenase-2 (COX-2) selective NSAIDs, and Diclofenac, a preferential COX-2 inhibitory NSAID, had shown uniformly the chemopreventive and anti-neoplastic effects in the early stage of colon cancer by promoting apoptosis as well as an over-expression of GSK-3β while down-regulating the PI3-K/Akt oncogenic pathway.
Thus, in addition to inhibitors of mPGES‑1 expression, EP4 antagonists and AKT/GSK-3β inhibitors may emerge as potential therapeutics to reduce CCR7 expression in colon cancer.
A colon cancer-derived mutant of Krüppel-like factor 5 (KLF5) is resistant to degradation by glycogen synthase kinase 3β (GSK3β) and the E3 ubiquitin ligase F-box and WD repeat domain-containing 7α (FBW7α).
Tissue microarray analysis of colon carcinoma samples from 5FU-treated patients revealed that GSK3B is significantly more activated in drug-resistant versus responsive patients.