Figure 2
Mutation of NF-κB or AP-1 binding site attenuated LMP1-increased iE κ activity. (A) Schematic diagram of mutant iEκ constructs were shown. The expansion for NF-κB or AP-1 binding site gave its wild-type sequence and the nucleotides replaced by mutations were underlined. Arrows indicated nucleotides introduced by mutations. (B) Comparison of the activities of iEκ in human nasopharyngeal carcinoma cell lines. Transient transfected the constructs carrying wild-type NF-κB and AP-1 sequences (pα-iEκwt), mutant NF-κB sequence (pα-iEκ-mtκB), mutant AP-1 sequence (pα-iEκ-mtAP-1), pGL3-α or pGL3-Basic into HNE2 and HNE2-LMP1 cells and luciferase reporter assays were performed as described in Materials and methods. The relative luciferase activity normalized to the value of the internal control plasmid pRL-SV40 activity. Results were expressed as fold induction of pGL3-Basic activity, which was assigned a value of 1. The data represent the mean ± SD of the three independent experiments performed in triplicate. Statistical significance: #P < 0.05 vs. pα-iEκwt-transfected HNE2, * P < 0.01 and ** P < 0.05 vs. pα-iEκwt-transfected HNE2-LMP1.