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. 2018 Mar 5;9(6):568–579. doi: 10.1007/s13238-018-0513-z

Figure 4.

Figure 4

Knock-down of Annexin A2 enhanced anti-proliferation effect of G-Rg5 and G-Rk1. (A) NF-κB activity was examined by luciferase reporter assay under treatment of G-Rg5 with (sh-Annexin A2) or without (sh-NC) knock-down of Annexin A2. (B and C) Activity of caspase 9 (B) and 3 (C) was examined under treatment of G-Rg5 with (sh-Annexin A2) or without (sh-NC) knock-down of Annexin A2. (D) Cell viability was examined by MTT for 48 h under treatment of G-Rg5 with (sh-Annexin A2) or without (sh-NC) knock-down of Annexin A2. (E) NF-κB activity was examined by luciferase reporter assay under treatment of G-Rk1 with (sh-Annexin A2) or without (sh-NC) knock-down of Annexin A2. (F and G) Activity of caspase 9 (F) and 3 (G) was examined under treatment of G-Rk1 with (sh-Annexin A2) or without (sh-NC) knock-down of Annexin A2. (H) Cell viability was examined by MTT for 48 h under treatment of G-Rk1 with (sh-Annexin A2) or without (sh-NC) knock-down of Annexin A2. (I) Plate clone formation assay was examined under treatment of G-Rg5 (6 μmol/L) and G-Rk1 (6 μmol/L) with (sh-Annexin A2) or without (sh-NC) knock-down of Annexin A2. (J) Protein level of Annexin A2 was examined by immunoblot with (sh-Annexin A2) or without (sh-NC) knock-down of Annexin A2, and β-actin was shown as a loading control. All data are shown as the mean ± SD. *P < 0.05, **P < 0.01 and ***P < 0.001 and the experimental points show the average of at least triplicates. All experiments were repeated at least 3 times. Statistical analyses were performed using Student’s t-test