SPI1 Mediates N-Myristoyltransferase 1 to Advance Gastric Cancer Progression via PI3K/AKT/mTOR Pathway

Figure 7

SPI1 regulated NMT1 via PI3K/AKT/mTOR pathway in GC cells. (a) The protein levels of PI3K, p-PI3K, AKT, p-AKT, mTOR, and p-mTOR in AGS cells were tested by western blot after transfection of NMT1 overexpression plasmid and shSPI1. GAPDH was the loading control. (b) The levels of p-PI3K/PI3K, p-AKT/AKT and p-mTOR/mTOR in AGS cells were tested by western blot after transfection of NMT1 overexpression plasmid and shSPI1. GAPDH was the loading control. (c) The protein levels of PI3K, p-PI3K, AKT, p-AKT, mTOR, and p-mTOR in SNU-5 cells were tested by western blot after transfection of shNMT1 and SPI1 overexpression plasmid. GAPDH was the loading control. (d) The levels of p-PI3K/PI3K, p-AKT/AKT and p-mTOR/mTOR in SNU-5 cells were tested by western blot after transfection of shNMT1 and SPI1 overexpression plasmid. GAPDH was the loading control. ^∗ < 0.05, ^∗∗ < 0.01, ^∗∗∗ < 0.001 vs. NC + shNC group; ^∧ < 0.05, ^∧∧∧ < 0.001 vs. NMT1+shNC group; ^# < 0.05, ^## < 0.01, ^### < 0.001 vs. NC + shSPI1 group; ⁺⁺ < 0.01, ⁺⁺⁺ < 0.001 vs. shNMT1+NC group; ^△△ < 0.01, ^△△△ < 0.001 vs. shNC + SPI1 group. All experiments were repeated independently at least three times. Data were performed as the means ± standard deviation. NMT1, N-myristoyltransferase 1; GC, gastric cancer; p-, phosphorylation; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; shNMT1, short hairpin RNA against NMT1; NC, negative control; shNC, shRNA negative control.

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