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

Figure 6.

Figure 6

Annexin A2-K302A protected cells from 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 Annexin A2-WT-myc and Annexin A2-K302A-myc overexpressed in HepG2 cells. (B and C) Activity of caspase 9 (B) and 3 (C) was examined under treatment of G-Rg5 with Annexin A2-WT-myc and Annexin A2-K302A-myc overexpressed in HepG2 cells. (D) Cell viability was examined by MTT for 48 h under treatment of G-Rg5 with Annexin A2-WT-myc and Annexin A2-K302A-myc overexpressed in HepG2 cells. (E) NF-κB activity was examined by luciferase reporter assay under treatment of G-Rk1 with Annexin A2-WT-myc and Annexin A2-K302A-myc overexpressed in HepG2 cells. (F and G) Activity of caspase 9 (F) and 3 (G) was examined under treatment of G-Rk1 with Annexin A2-WT-myc and Annexin A2-K302A-myc overexpressed in HepG2 cells. (H) Cell viability was examined by MTT for 48 h under treatment of G-Rk1 with Annexin A2-WT-myc and Annexin A2-K302A-myc overexpressed in HepG2 cells. (I) Plate clone formation assay was examined under treatment of G-Rg5 (6 μmol/L) and G-Rk1 (6 μmol/L) with Annexin A2-WT-myc and Annexin A2-K302A-myc overexpressed in HepG2 cells. All data are shown as the mean ± SD and the experimental points show the average of at least triplicates. All experiments were repeated at least 3 times