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. 2016 Feb 5;7(10):11463–11477. doi: 10.18632/oncotarget.7201

Figure 6. RKIP-regulated NPC cell radioresponse is mediated through ERK and AKT signaling.

Figure 6

(A) (left) a representative result of Western blotting shows the levels of the phospho-ERK-1/2, phospho-AKT and RKIP in the RKIP KD CNE2 treated with a range of 5–20 μmol/L MEK inhibitor U0126; (right) a representative result of Western blotting shows the levels of phospho-ERK-1/2, phospho-AKT and RKIP in the RKIP OE CNE2-IR cells transfected with 4 μg/mL ERK-2 expression vector (OE). (B) a clonogenic survival assay shows that inhibition of ERK and AKT signaling significantly abrogated CNE2 KD cell radioresistance induced by RKIP knockdown. Cells treated with 10 μmol/L U0126, 10 μmol/L LY294002 or 2 μmol/L AKT-1 DNAzyme were irradiated with a range of 1–8Gy radiation doses, and dose survival curves were created by fitting surviving fractions to the linear quadratic equation. (C) a clonogenic survival assay shows that activation of ERK and AKT signaling restored CNE2-IR OE cell radioresistance reduced by RKIP overexpression. Cells transfected with 4 μmol/L of ERK-2 or AKT-1 expression plasmid were irradiated with a range of 1–8Gy radiation doses, and dose survival curves were created by fitting surviving fractions to the linear quadratic equation. (C) Spearman rank correlation analysis shows that RKIP level was negatively associated with phospho-ERK−1/2 level (a) and phospho-AKT level (b), and phospho-ERK−1/2 level was positively associated with phospho-AKT level in 149 cases of NPCs. OE, overexpression; KD, knockdown.