Fig. 5

AGK increases the population of EOC CSC and induces chemoresistant in vivo. A Flow cytometry analysis of annexin V⁺/PI ̄ cells after the indicated cells were treated with cisplatin (40 μm/ml, 80 μm/ml, 120 μm/ml) for 24 h. Results were expressed as percentages of total cells. B The dose-dependent curve of cisplatin treatment for OVCAR3-AGK and OVCAR3-Vector cells. C Cleaved caspase 3, caspase 3, Bcl-2, p-P53, and P53 were apoptosis markers tested by WB. D Cisplatin chemoresistance of AGK on EOC in vivo. AGK-overexpressing (OVCAR3-AGK) or AGK-knockdown (OVCAR3-AGKshRNA) cells (5 × 10⁶) were injected subcutaneously into the subcutaneous and intraperitoneal inguinal folds of NOD/SCID mice. 3 days later, cisplatin (5 mg/kg) was injected intraperitoneally into nude mice 3 times per week. On Day 25, mice were euthanized and the tumors as well as ascites were excised and weighed. A chemiluminescent imaging system (Sacecreation) was used to evaluate the tumors in the mice. Error bars represent the means ± SD of 3 independent experiments. *P < 0.05. **P < 0.001. N = 3 independent experiments