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

Figure 7 Tumor cell-derived BIRC3 inhibits apoptosis by activating AKT pathway, lead to drug resistance to trastuzumab. A: Experimental in Balb/c nude mice. Tumor volume images, tumor weight and tumor growth curves of each group were shown. The different treatment groups included: (1) The stable control NCI-N87 cells (N87 group); (2) The stable BIRC3 overexpressing NCI-N87 cells with the trastuzumab treatment (N87-LV-BIRC3 group); and (3) The NCI-N87 transfected with the overexpressed virus LV-GFP-puro-BIRC3 and treated with AKT inhibitor (MK-2206) (N87-LV-BIRC3-AKTi group); B: (1) The NCI-N87 was developed into a trastuzumab-resistant cell line(N87R group); (2) The group inoculated with NCI-N87R cells transfected with the knockout virus LV-GFP-puro-BIRC3-si (N87-LV-BIRC3 group); C and D: Immunohistochemistry staining for BIRC3, pAKT and caspase 3 was presented, and the immunohistochemistry scores for BIRC3, pAKT and caspase 3 were statistically analyzed. IHC: Immunohistochemistry; HE: Hematoxylin-eosin; NS: No significance.