Fig. 6

Requirement of EID3 for the stemness of gastric cancer stem cell-like cells. A Role of EID3 in the proliferation of radiotherapy-induced, chemotherapy-induced or sorted GCSCs. GCSCs were transfected with EID3-siRNA. As a control, siRNA control was included in the transfection. At different time after transfection, the cell proliferation was examined. The statistical significance of difference between treatments was indicated with asterisks (*p < 0.05; **p < 0.01). B Effects of EID3 silencing or rescue on cell cycle of radiotherapy-induced, chemotherapy-induced or sorted GCSCs. Thirty-six hours after the treatment of EID3-siRNA or rescue, GCSCs were subjected to cell cycle analysis (*p < 0.05; **p < 0.01). C Impact of EID3 silencing or rescue on the caspase 3/7 activity of GCSCs. GCSCs were treated with EID3-siRNA or EID3 rescue. Thirty-six hours after treatment, the caspase 3/7 activity of cells was examined (**p < 0.01). D Evaluation of apoptosis using annexin V assays. Thirty-six hours after treatment, apoptosis of GCSCs was examined using flow cytometry (**p < 0.01). E Role of EID3 in the therapy resistance of gastric cancer stem cell-like cells (GCSCs). GCSCs (cisplatin-induced, doxorubicin-induced, X-ray-induced or sorted GCSCs) were transfected with EID3-siRNA, siRNA control or EID3-siRNA + plasmid expressing EID3. At different time after transfection (0, 24, 36 and 48 h), GCSCs were treated with cisplatin (300 μM, 24 h), doxorubicin (1 μM, 24 h) or X-ray (20 Gy). Subsequently, the cell viability was examined (*p < 0.05; **p < 0.01)