Research Paper Volume 14, Issue 9 pp 3887—3909

Figure 10. ILF3 was involved in the regulation of PI3K/AKT/mTOR signaling pathway in gastric cancer cell SGC-7901. (A:ox-LDL+si-nc;B:ox-LDL+si-ILF3;C:ox-LDL+statin;D:ox-LDL+CMV-2;E:ox-LDL+flag-ILF3;F:ox-LDL+flag-ILF3+PI3K/AKT inhibitor LY294002). (A–C) ILF3-specific small interference RNA (si-ILF3) and statins treatment significantly inhibited PI3K/AKT/mTOR signaling pathway. The expression of p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR were significantly downregulated compared to control group. And the expression of PI3K, Akt and mTOR and p-mTOR did not change significantly. (D–F) ILF3-overexpressed plasmids (flag-ILF3) treatment significantly activated PI3K/AKT/mTOR signaling pathway. The expression of p-PI3K/PI3K, p-AKT/AKT, and p-mTOR/mTOR were significantly upregulated compared to vector plasmids (CMV2) group. PI3K/AKT inhibitor LY294002 treatment significantly inhibited the PI3K/AKT/mTOR signaling pathway.