Research Paper Volume 14, Issue 9 pp 3887—3909

Ox-LDL-mediated ILF3 overexpression in gastric cancer progression by activating the PI3K/AKT/mTOR signaling pathway

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Figure 6. ILF3 promotes gastric cancer cells proliferation, cell cycle, migration, and invasion, and statins may exert an anti-tumor effect by inhibiting ILF3 expression in gastric cancer. (A) Statins inhibited the expression of ILF3 in a concentration-dependent manner, the optimal concentration was 40&mu;mol/L. The protein expression of ILF3 was significantly downregulated with ILF3-specific small interference RNA (si-ILF3) and statin treatment compared to control group. The expression level of ILF3 was analyzed with western blot. (B) Edu assay analyzed the effects of ILF3 on cell proliferation of gastric cancer cells. ILF3-specific small interference RNA (si-ILF3) and statins treatment inhibited the proliferation of HGC-27 and Ncl-N87 cells compared to control group. (C) The protein expression of PCNA was lower expressed in the ILF3-specific small interference and statins treatment groups compared to control group. (D) Flow cytometry analyzed the effect of ILF3 on cell cycle of gastric cancer cells. ILF3-specific small interference RNA (si-ILF3) and statins treatment inhibited the cell cycle of HGC-27 and Ncl-N87 cells compared to control group. (E) The protein expression of cyclin-D1 was lower expressed in the ILF3-specific small interference and statins treatment groups compared to control group. (F) Transwell assay analyzed the effect of ILF3 on cell migration and invasion. ILF3-specific small interference RNA (si-ILF3) and statins treatment inhibited the migration and invasion of HGC-27 and Ncl-N87 cells compared to control group. (G) The protein expression of MMP-2 and MMP-9 were lower expressed in the ILF3-specific small interference and statins treatment groups compared to control group. **P < 0.01, ***P < 0.001, ****P < 0.0001.