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lüll Melanoma differentiation associated gene-7/interleukin-24 promotes tumor cell-specific apoptosis through both secretory and nonsecretory pathways Sauane M; Lebedeva IV; Su ZZ; Choo HT; Randolph A; Valerie K; Dent P; Gopalkrishnan RV; Fisher PBCancer Res 2004[May]; 64 (9): 2988-93Melanoma differentiation associated gene-7/interleukin-24 (Mda-7/IL-24), a novel member of the IL-10 family of cytokines, uniquely displays cancer-specific apoptosis-inducing activity. Positive results in ongoing phase I/II clinical trials have strengthened the possibility of its utilization as a cancer gene therapeutic. Previous studies document that signaling events leading to Ad.mda-7-induced transformed cell apoptosis are tyrosine kinase-independent. These results suggest that mda-7/IL-24 cancer cell-specific activity could occur through mechanisms independent of binding to its currently recognized cognate receptors and might even occur independent of receptor function. An adenovirus vector expressing a nonsecreted version of MDA-7/IL-24 protein was generated via deletion of its signal peptide. This nonsecreted protein was as effective as wild-type secreted MDA-7/IL-24 in inducing apoptosis in prostate carcinoma cell lines and displayed transformed cell specificity and localization of MDA-7/IL-24 in the Golgi/endoplasmic reticulum compartments. Our results indicate that mda-7/IL-24-mediated apoptosis can be triggered through a combination of intracellular as well as secretory mechanisms and can occur efficiently in the absence of protein secretion.|Adenoviridae/genetics[MESH]|Apoptosis/genetics/*physiology[MESH]|Cell Division/genetics/physiology[MESH]|Cell Line, Tumor[MESH]|Endoplasmic Reticulum/metabolism[MESH]|Genes, Tumor Suppressor[MESH]|Genetic Therapy/methods[MESH]|Genetic Vectors/genetics[MESH]|Golgi Apparatus/metabolism[MESH]|Humans[MESH]|Interleukins/genetics/metabolism/*physiology[MESH]|Male[MESH]|Mitogen-Activated Protein Kinase 1/metabolism[MESH]|Mitogen-Activated Protein Kinase 3[MESH]|Mitogen-Activated Protein Kinases/metabolism[MESH]|Neoplasm Invasiveness[MESH]|Prostatic Neoplasms/genetics/metabolism/pathology/therapy[MESH] |