Liver Cancer
Copyright ©2007 Baishideng Publishing Group Co.
World J Gastroenterol. Feb 7, 2007; 13(5): 683-691
Published online Feb 7, 2007. doi: 10.3748/wjg.v13.i5.683
Figure 2
Figure 2 Selective replication of CNHK500-p53 in vitro. A: Human HCC cell lines HepG2, Hep3B, and SMMC-7721 were infected with CNHK500-p53 at a MOI of 5. Cells and media were harvested, and lysates were prepared from each group at diverse time points 0 h, 24 h, 48 h, and 96 h. Viral titers were measured with the tissue culture infectious dose 50 method, normalized with that at the beginning of infection, and shown as multiples. CNHK500-p53 replicated similarly as CNHK500 and WtAd5 in all of the tested telomerase-positive cancer cells; B: Comparison of replication capability of CNHK500-p53, CNHK500 and WtAd5 in telomerase-negative normal cell lines. At diverse time points 0 h, 24 h, 48 h, and 96 h after infection, cells and medium were harvested, and viral titers were measured as described previously. In all of the tested normal cell lines, the replication capability of CNHK500-p53 and CNHK500 was severely attenuated than that of WtAd5; C: Forty-eight hours after infection with CNHK500-p53 in HepG2, Hep3B and BJ, CNHK500-p53 showed enhanced replication ability both in HepG2, Hep3B and in BJ under hypoxia condition, but was higher in HepG2, Hep3B than in BJ.