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. 2016 Mar 18;7(16):22733–22745. doi: 10.18632/oncotarget.8174

Figure 2. Knockdown of Bmi-1 by Ad-Bmi-1i transfection decreases malignant phenotypes in GC cells in vitro.

Figure 2

(A) Knockdown of Bmi-1 decreases proliferative ability detected by plate colony formation assay in stably Bmi-1 knockdown SGC-7901 and HGC-27 cells. (B) Knockdown of Bmi-1 results in induction of cellular senescence. Cellular senescence was stained using SA-β-gal assay in SGC-7901 (left) and HGC-27 (right) cells, stable Bmi-1 knockdown (Ad-Bmi-1i) or control vector (Ad-Ctrli) (upper), and quantified (lower). (C) Knockdown of Bmi-1 in SGC-7901 results in slightly increase of cellular apoptosis in vitro detected by the Annexin V-propidium iodide apoptosis detection. (D) Bmi-1 inhibition induced by Ad-Bmi-1i reduced gastric CSC self-renewal activity in vitro. Bmi-1 knockdown cells and its control cells were cultured using serum-free microsphere culture method. (E) Bmi-1 knockdown sensitizes gastric cancer cells to chemotherapy in SGC-7901 cells. Bmi-1 knockdown cells and its control cells were treated with 5-fluorouracil detected by CCK8 after 48 hours. For a dose-dependent assay, the cells were administered with different doses of 5-fluorouracil, and cell survival was determined 48 hours after administration. (F) Bmi-1 knockdown inhibits migration in SGC-7901 cells. Transwell migration assay was performed using the Corning Transwell chamber (8 μm), pictures of migrated cells was showed in left panel, and quantitation of migrated cells in right panel. (data are represented as mean ± SD) *P < 0.05, **P < 0.01.