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. 2021 Apr 14;125(2):220–228. doi: 10.1038/s41416-021-01366-1

Fig. 3. GNG4 promotes malignant phenotypes of gastric cancer cell lines; in vitro and in vivo assays with transient overexpression of GNG4 (oeGNG4) and stable knockout of GNG4 (dGNG4).

Fig. 3

Cell proliferation assay (a) and mitochondrial membrane depolarisation (MitoPotential) assay (b) between N87 cells transfected with an empty vector (N87-empty) and N87-oeGNG4 cells. Cell proliferation assay (c) and MitoPotential assay (d) between parental MKN1 and dGNG4-MKN1 cells. Cell cycle assay comparing MKN1 and dGNG4-MKN1 cells using colorimetric detection of the cell cycle phase (e). Drug-sensitivity assay to 5FU (f) and cell adhesion assay to solid matrices (g) comparing MKN1 and dGNG4-MKN1 cells. Capillary-based immunoassays of phospho-extracellular signal-regulated kinase 1/2 (ERK1/2) (Thr202/Tyr204), total ERK1/2, phospho-Akt (Ser473) and total Akt comparing MKN1 and dGNG4-MKN1 cells (h). p- indicates phosphorylated; t-, total. Mouse subcutaneous xenograft model (i) and liver metastatic model (j) comparing MKN1 and dGNG4-MKN1 cells. Tumour volume was evaluated with an in vivo spectrum imaging system (IVIS) at 4, 8 and 12 weeks after implantation (plotted chronologically in the lower panel) and by MRI at 12 weeks after implantation. Circles on the mice indicate regions of interest. *P < 0.05, **P < 0.01, ***P < 0.001.