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. 2016 Nov 24;6:37717. doi: 10.1038/srep37717

Figure 4. HBx upregulates SATB1 expression through the JNK and ERK pathway and the activation of c-Jun.

Figure 4

(a) L02-HBx, CHL-HBx cells and corresponding control groups L02-Vector, L02-WT, CHL-Vector, CHL-WT were respectively treated with specific JNK inhibitor SP600125 (25 uM), ERK1/2 inhibitor U0126 (25 uM), PI3K inhibitor Ly294002 (25 uM), p38 inhibitor SB203580 (25 uM) for 48 hours. Protein levels of SATB1, c-Jun, phosphorylated and total JNK, ERK1/2, p38 and Akt were analyzed by western blot. Full-length blots are included in the Supplementary Fig. S8. (b) Real-time PCR analysis of SATB1 expression in L02-HBx, CHL-HBx cells and corresponding control groups after transfection with siRNA targeting various transcription factors c-Jun, Sp1, NFKB1 for 48 hours, respectively. (n = 3). *P < 0.05, **P < 0.01 vs. L02-HBx NC or CHL-HBx NC. (c) Protein levels of SATB1, c-Jun, Sp1, NFKB1 were analyzed by western blot. Full-length blots are included in the Supplementary Fig. S8. (d) SATB1 promoter reporter vectors were contransfected with siRNA targeting various transcription factors c-Jun, Sp1, NFKB1 into L02-HBx and CHL-HBx cells, respectively. The SATB1 promoter activity was measured at 72 h posttranscfection. (n = 3). *P < 0.05, **P < 0.01 vs. L02-HBx NC or CHL-HBx NC.