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lüll mda-7/IL-24 induces apoptosis in human GBC-SD gallbladder carcinoma cells via mitochondrial apoptotic pathway Jia J; Li S; Gong W; Ding J; Fang C; Quan ZOncol Rep 2011[Jan]; 25 (1): 195-201mda-7/IL-24 has tumor-suppressor activity in a broad spectrum of human cancer cells. However, the therapeutic effect of the recombinant human IL-24 protein on human gallbladder carcinoma has rarely been explored. In this study, we used a human gallbladder carcinoma cell line (GBC-SD) to explore the effect of adenovirus-mediated IL-24 (Ad-IL24) gene therapy on GBC-SD cells. We show that Ad-IL24 treatment of GBC-SD cells in vitro conspicuously induced apoptosis of GBC-SD cells. We also demonstrate that the in vivo treatment of GBC tumor-bearing athymic nude mice intratumorally injected with Ad-IL24 significantly suppressed GBC growth. To further explore the mechanism that mda-7/IL-24 utilized in tumor cell apoptosis, we examined molecules and pathways involved in apoptotic regulation and found that Ad-IL24 induced the down-regulation of anti-apoptotic gene Bcl-2 and the release of cytochrome c, which subsequently activated caspase-9, caspase-3 and PARP to induce apoptosis. In summary, adenovirus (AdV)-mediated IL-24 overexpression exerted potent antitumor activity via stimulating mitochondrial apoptotic pathway in GBC-SD. Therefore, mda-7/IL-24 has the potential to serve as a tool for targeted gene therapy in the treatment of gallbladder cancer.|Adenoviridae/genetics[MESH]|Animals[MESH]|Apoptosis/*genetics[MESH]|Blotting, Western[MESH]|Carcinoma/*genetics/metabolism/pathology[MESH]|Cell Line, Tumor[MESH]|Gallbladder Neoplasms/*genetics/metabolism/pathology[MESH]|Gene Expression Regulation, Neoplastic/genetics[MESH]|Genes, bcl-2[MESH]|Genetic Therapy/*methods[MESH]|Genetic Vectors[MESH]|Humans[MESH]|Interleukins/*genetics/metabolism[MESH]|Mice[MESH]|Mice, Nude[MESH]|Mitochondria/*metabolism[MESH]|Reverse Transcriptase Polymerase Chain Reaction[MESH]|Xenograft Model Antitumor Assays[MESH] |