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Enhancement of adenoviral MDA-7-mediated cell killing in human lung cancer cells by geldanamycin and its 17-allyl- amino-17-demethoxy analogue Pataer A; Bocangel D; Chada S; Roth JA; Hunt KK; Swisher SGCancer Gene Ther 2007[Jan]; 14 (1): 12-8Our previous studies demonstrated that adenovirus-mediated overexpression of melanoma differentiation-associated gene-7 (Ad-mda7) leads to rapid induction of double-stranded RNA-dependent protein kinase (PKR) and activation of its downstream targets, resulting in apoptosis induction in human lung cancer cells. Here, we report that Ad-mda7 and the benzoquinone ansamycin geldanamycin (GA) interact in a highly synergistic manner to induce cell death in human lung cancer cells. Co-administration of Ad-mda7 and GA did not modify expression of MDA-7, and was not associated with further PKR induction and activation; instead the enhanced cytotoxicity of this combination was associated with inactivation of AKT by GA. By surface staining using anti-E-cadherin monoclonal antibody and flow cytometry, we found that treatment with the combination of Ad-mda7 and GA increased E-cadherin levels in these cancer cells. Ad-mda7 and GA cotreatment also inhibited lung cancer cell motility by increasing the beta-catenin/E-cadherin association. Moreover, combination of GA derivative 17-allyl-amino, 17-demethoxygeldanamycin (17AAG), with Ad-mda7 resulted in enhancement of cell death in A549 and H460 human lung cancer cells.|Adenoviridae/*genetics[MESH]|Benzoquinones/chemistry/*pharmacology[MESH]|Blotting, Western[MESH]|Cell Line, Tumor[MESH]|Cell Survival/*drug effects[MESH]|Flow Cytometry[MESH]|Fluorescent Antibody Technique[MESH]|Genetic Vectors[MESH]|Humans[MESH]|Lactams, Macrocyclic/chemistry/*pharmacology[MESH]|Lung Neoplasms/*pathology[MESH]|Protein Kinase Inhibitors/*pharmacology[MESH]|Protein-Tyrosine Kinases/*antagonists & inhibitors[MESH] |
