Fig. 5.

Enhanced expression of NS1-BP suppresses MYC signaling by transcriptionally inhibiting c-Myc. a Western blot showing the expression of key downstream factors of the MYC signaling pathway. All data were derived from three independent experiments. b c-Myc phenotype reversal in NS1-BP-overexpressing cells restored the expression of survivin, CDK4, and p27. c Western blot showing that ectopic NS1-BP expression attenuated irradiation-induced activation of the ATM/Chk1 pathway (ATM^p phosphorylated ATM, Chk1^p phosphorylated Chk1, Chk2^p phosphorylated Chk2). d Analysis of luciferase activity. Fragment containing c-Myc promoter region sequence was cloned downstream of the luciferase reporter gene. Plasmids were transfected into empty vectors or NS1-BP stably expressing cells. Renilla luciferase plasmids were co-transfected for normalization. Data are the mean ± SD of three independent experiments (**P < 0.01). e ChIP assay on ESCC cellular extracts using NS1-BP antibodies followed by RT-PCR to analyze the associated c-Myc promoter region. (NC non-related c-Myc promoter negative control)