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. 2016 Apr 1;7(18):26516–26534. doi: 10.18632/oncotarget.8530

Figure 7. miR-520g increased chemoresistance to cisplatinum and paclitaxel and inhibited EOC cell viability by repressing DAPK2.

Figure 7

(A) A2780/vector cells and A2780/miR-520g cells transfected with the Lv-DAPK2 or control vectors, respectively, were treated with PBS, cisplatin (10 μl) and paclitaxel (50 μl) for 36 hours. Apoptosis. Was analyzed using Annexin V/PI staining and FACS. DAPK2 overexpression decreased chemoresistance induced by miR-520g and increased sensitivity to cisplatin and paclitaxel. (B) MCAS/NC cells and MCAS/Anti-miR-520g cells were transfected with DAPK2/siRNA or scramble, respectively, and then treated with PBS, cisplatin (10 μl) and paclitaxel (50 μl) for 36 hours. Apoptosis. Was analyzed using Annexin V/PI staining and FACS. DAPK2 knockdown partially inhibited chemosensitivity induced by miR-520g knockdown. (C) After transfection with Lv-DAPK2 or control vectors, A2780/miR-520g-vector cells and A2780/miR-520g cells were treated with cisplatin and paclitaxel for 36 h. DAPK2 overexpression decreased cell viability promoted by miR-520g as measured by CCK8 assay (*p < 0.05, **p < 0.001). (D) Following transfection with DAPK2siRNA or scramble, MCAS/NC cells and MCAS/Anti-miR-520g cells were treated with cisplatin and paclitaxel for 36 h. DAPK2 knockdown partially restored cell viability (*p < 0.05, **p < 0.001). (E) Western blot analysis for caspase-3 and poly (ADP-ribose) polymerase (PARP) in A2780/vector cells and A2780/miR-520g cells transfected with the Lv-DAPK2 or control vectors, respectively, and treated with PBS, cisplatin (10 μl) and paclitaxel (50 μl) for 36 hours. (F) Western blot analysis for caspase-3 and PARP in MCAS/NC cells and MCAS/Anti-miR-520g cells transfected with the DAPK2/siRNA or scramble, respectively, and treated with PBS, cisplatin (10 μl) and paclitaxel (50 μl) for 36 hours.