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

Figure 2

NMT1 was upregulated in GC cells and modulated GC cell viability. (a) NMT1 mRNA expression between human GC cell lines (AGS, HGC27, SNU-5, and MKN-45) and normal cell line GES-1 was detected through qRT-PCR. GAPDH was the loading control. (b) NMT1 protein expression between human GC cell lines (AGS, HGC27, SNU-5, and MKN-45) and normal cell line GES-1 was tested by western blot. GAPDH was the loading control. (c) NMT1 mRNA expression of AGS cells was detected through qRT-PCR after transfection of NMT1 overexpression plasmid. GAPDH was the loading control. (d) NMT1 mRNA expression of SNU-5 cells was detected through qRT-PCR after transfection of shNMT1. GAPDH was the loading control. (e) OD value of AGS cells at 24, 48, or 72 h was assessed by MTT assay after transfection of NMT1 overexpression plasmid. (f) OD value of SNU-5 cells at 24, 48, or 72 h was assessed by MTT assay after transfection of shNMT1. ^∗∗∗ < 0.001 vs. GES-1 cells;^∧ < 0.05, ^∧∧∧ < 0.001 vs. NC group; ^# < 0.05, ^## < 0.01, ^### < 0.001 vs. shNC 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.

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