作者: Gerald M. Fuller , Gene P. Siegal , Minghui Wang , David T. Curiel , Simon A. Jones
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摘要: In this study, we report that an interleukin-6 (IL-6)-inducible E1A-substituting activity can be exploited for the production of infectious adenoviral particles during infection with E1A-deleted adenovirus (Ad) Ad5dl312. The basal level complementation increased by 1.5 log induction HepG2 cells recombinant human IL-6. Additionally, IL-6-inducible complement E1A deletion in other cancer cell lines to render them Ad producer on IL-6, although efficiency varies between lines. Ad5dl312 replicate in, produce cytotoxic effect, and kill tumor without addition exogenous IL-6 context possessing autocrine arc, such as ovarian cells. contrast, normal mesothelial isolated from peritoneum lining do not support replication Ad5dl312, even presence These results suggest could used a agent selectively responsive or arc.