Fig. 5

Inhibition of ESPL1 enhances the sensitivity of GC cells to apatinib. a Predicting the targeted therapeutics response for ESPL1 high expression group and low expression group of GC based on the Genomics of Drug Sensitivity in Cancer (GDSC); b, c The AGS cell lines were transfected with ESPL1 knockdown plasmid, q-PCR(b) and (c) was used to detect the knockdown efficiency of shESPL1; d CCK8 assay was used to detect cell proliferation after treated with 0, 1, 10 and 40 μg/mL apatinib of AGS-shNC and AGS-shESPL1 cells; e, f Transwell assays clearly revealed the invasion cells in AGS-shNC and AGS-shESPL1 group after treated with 10 μg/mL apatinib for 48 h; g, h Apoptosis assays showed the proportion of apoptotic cells in AGS-shNC and AGS-shESPL1 group after treated with 10 μg/mL apatinib for 48 h; i Western blots was conducted to detect p-AKT, VEGF and BCL-2 protein levels in AGS-shNC and AGS-shESPL1 group after treated with 10 μg/mL apatinib for 48 h(left), the Image J software was used for quantitative analysis(right). Statistical significance was determined by One-way ANOVA. Data were represented as means ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 compared with the NC group