Fig. 3

GPAA1 promotes the metastasis and invasion of gastric cancer. a GSEA of specimens with high and low expression of GPAA1 based on the data from GES66229 (ALONSO_METASTASIS, NES = 1.539, P = 0.001, FDR = 0.202; KEGG_GPI_ANCHOR_BIOSYNTHESIS, NES = 1.554, P = 0.012, FDR = 0.143. b-c WB analysis of PSCA, UPAR, C4.4A, MMP2, MMP9, and MMP14 in the GPAA1-upregulated, GPAA1-downregulated, and control groups. d Wound healing assays were conducted using GPAA1-knockdown, GPAA1-overexpressing and control AGS and MKN-45 cells (Scale bar: 100 μm), and the percentage of wound closure was calculated from the widths of the wound at 0 h and 48 h. The means ± SDs of three independent experiments are shown. e Transwell assays were performed with GPAA1-knockdown, GPAA1-overexpressing and control SGC-7901 and HGC-27 cells to assess the migration and invasive abilities (Scale bar: 50 μm). The number of cells migrating through the inserts was calculated, and the means ± SDs of three independent experiments are shown. f The overexpression efficiency of GPAA1 in MFC cells was tested by western blotting. g The overexpression efficiency of GPAA1 in MFC cells was assessed by immunofluorescence staining. h Experimental design of the in vivo study to explore the regulation of liver metastasis by GPAA1 in mice. i Liver metastasis in the Lv-Ctrl and Lv-GPAA1 groups was verified via the IVIS system and quantified by the total flux. *P < 0.05, **P < 0.01, ***P < 0.001