Research Paper Volume 13, Issue 16 pp 20738—20747

Apatinib inhibits the proliferation of gastric cancer cells via the AKT/GSK signaling pathway in vivo

The inhibition effect of apatinib on the cell viability in different GC cell lines. (A) Cell viability of different human gastric cancer cell lines treated with different concentrations of apatinib for 72 h. (B) After treatment with apatinib 2 μM concentration for 72 h, western blot analysis of AKT, phosphorylated AKT (p-AKT), GSK3α, phosphorylated GSK3α (p-GSK3α), GSK3β and phosphorylated GSK3β (p-GSK3β) in GC cell lines. (C) Cell viability of different human gastric cancer cell lines treated with different concentrations of apatinib for 8 h. (D) After treatment with apatinib 2 μM concentration for 8 h, western blot analysis of AKT, phosphorylated AKT (p-AKT), GSK3α, phosphorylated GSK3α (p-GSK3α), GSK3β and phosphorylated GSK3β (p-GSK3β) in GC cell lines.

Figure 1. The inhibition effect of apatinib on the cell viability in different GC cell lines. (A) Cell viability of different human gastric cancer cell lines treated with different concentrations of apatinib for 72 h. (B) After treatment with apatinib 2 μM concentration for 72 h, western blot analysis of AKT, phosphorylated AKT (p-AKT), GSK3α, phosphorylated GSK3α (p-GSK3α), GSK3β and phosphorylated GSK3β (p-GSK3β) in GC cell lines. (C) Cell viability of different human gastric cancer cell lines treated with different concentrations of apatinib for 8 h. (D) After treatment with apatinib 2 μM concentration for 8 h, western blot analysis of AKT, phosphorylated AKT (p-AKT), GSK3α, phosphorylated GSK3α (p-GSK3α), GSK3β and phosphorylated GSK3β (p-GSK3β) in GC cell lines.