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

Figure 5

SPI1 regulated NMT1 to mediate GC cell viability. (a, b) SPI1 expression (a) and NMT1 mRNA expression (b) of AGS cells were detected through qRT-PCR after transfection of NMT1 overexpression plasmid and shSPI1. GAPDH was the loading control. (c, d) The mRNA expressions of SPI1 (c) and NMT1 (d) of SNU-5 cells were detected through qRT-PCR after transfection of shNMT1 and SPI1 overexpression plasmid. GAPDH was the loading control. (e) OD value of AGS cells at 48 h was assessed through MTT assay after transfection of NMT1 overexpression plasmid and shSPI1. (f) OD value of SNU-5 cells at 48 h was assessed through MTT assay after transfection of shNMT1 and SPI1 overexpression plasmid. ^∗ < 0.05, ^∗∗ < 0.01, ^∗∗∗ < 0.001 vs. NC + shNC group; ^∧∧ < 0.01, ^∧∧∧ < 0.001 vs. NMT1+shNC group; ^# < 0.05, ^## < 0.01 vs. NC + shSPI1 group; ⁺ < 0.05, ⁺⁺ < 0.01, ⁺⁺⁺ < 0.001 vs. shNMT1+NC group; ^△ < 0.05, ^△△△ < 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; qRT-PCR, quantitative reverse transcription-polymerase chain reaction; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; shNMT1, short hairpin RNA against NMT1; OD, optical density; NC, negative control; shNC, shRNA negative control.

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