BIRC3 induces the phosphoinositide 3-kinase-Akt pathway activation to promote trastuzumab resistance in human epidermal growth factor receptor 2-positive gastric cancer

Figure 6 Tumor cell-derived BIRC3 enhancing the proliferation of human epidermal growth factor receptor 2-positive gastric cancer cell treated with trastuzumab activating AKT pathway. BIRC3 siRNA or siRNA-NC was transfected into NCI-N87R cells (designated as N87R-siRNA and N87R-siNC). NCI-N87 cells were pretreated with an Akt inhibitor (MK-2206) and transfected with the overexpression plasmid pLVX-IRES-puro-BIRC3 (designated as N87-AKTi-OE). A: Revealed that the differential genes were mainly enriched in pathways by the Kyoto encyclopedia of genes and genomes enrichment analysis; B: Protein levels of BIRC3 and AKT, p-AKT were examined by western blotting. β-actin was a negative control; C: Cell viabilities of N87, N87-BIRC3-OE and N87-BIRC3-NC cells 1000μg/mL trastuzumab were examined by cell counting kit-8 assay; D: Cell viabilities of N87, N87-BIRC3-OE and N87-BIRC3-NC cells 1000μg/mL trastuzumab were examined by 5-ethynyl-2’-deoxyuridine assay; E: Protein levels of BIRC3 and AKT, p-AKT in N87,N87-BIRC3-OE, and N87-AKTi-OE cells were examined by western blotting. β-actin was a negative control. Tra: Trastuzumab; EdU: 5-ethynyl-2’-deoxyuridine; NS: No significance.