dl 1520 inhibited the proliferation of GC cells by selectively replicating in and destroying the cancer cells. A, B) The efficiencies of infection and replication of dl 1520 in GC and normal cells. The infection efficiency (A) of dl 1520 was shown as the dl 1520 DNA copy number relative to β-actin at 0 hours after infection. The replication efficiency (B) of dl 1520 was presented as the fold of the dl 1520 DNA copy number at indicated time relative to that at 0 hours post-infection (One-way ANOVA, *p<0.05, **p<0.01 compared to that at 0 hours post-infection). C~E) The cytopathic effect (CPE) of dl 1520 on GC cells. MTT cell proliferation assays were used to analyze the CPE of dl 1520 on AGS (C), MGc80-3 (D) and SGC-7901 (E) GC cells. The results are presented as the percentages of viable cells related to the negative control (one-way ANOVA, *p<0.05, **p<0.01 compared to that at 0 MOIs). F) Western blotting analysis of protein levels of p14ARF in GC cells (Actin was used as the internal control). G) Quantitative RT-PCR analysis of the relative mRNA levels of p14ARF and p53 (normalized to that of GAPDH). H) The replication of dl 1520 after modifying the p14ARF levels by knockdown or overexpression. AGS cells were transfected with pCD-p14ARF plasmid (pcDNA3.1(+) as a negative control), and MGc80-3 cells were transfected with p14ARF siRNA (si-p14ARF) (scrambled siRNA as a negative control). The cells were analyzed p14ARF expression by Western blotting after 48 hours post-transfection (H upper). Or the cells were infected with 10 MOIs of dl 1520 after 24 hours post-transfection, and dl 1520 DNA copy numbers were analyzed in GC cells after 48 hours post-infection (normalized against that at 0 hours) (H lower). (Student’s t test, *p< 0.05 compared with their respective control).