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00925njm 22002777a 4500 dc Tormo, Damià author Checińska, Agnieszka author Alonso-Curbelo, Direna author Pérez-Guijarro, Eva author Cañón, Estela author Riveiro-Falkenbach, Erica author Calvo, Tonantzin G author Larribere, Lionel author Megías, Diego author Mulero, Francisca author Piris, Miguel A author Dash, Rupesh author Barral, Paola M author Rodríguez-Peralto, José L author Ortiz-Romero, Pablo author Tüting, Thomas author Fisher, Paul B author Soengas, MS author Tormo, Damià author Checińska, Agnieszka author Alonso-Curbelo, Direna author Pérez-Guijarro, Eva author Cañón, Estela author Riveiro-Falkenbach, Erica author Calvo, Tonantzin G author Larribere, Lionel author Megías, Diego author Mulero, Francisca author Piris, Miguel A author Dash, Rupesh author Barral, Paola M author Rodríguez-Peralto, José L author Ortiz-Romero, Pablo author Tüting, Thomas author Fisher, Paul B author 2009-08-04 Inappropriate drug delivery, secondary toxicities, and persistent chemo- and immunoresistance have traditionally compromised treatment response in melanoma. Using cellular systems and genetically engineered mouse models, we show that melanoma cells retain an innate ability to recognize cytosolic double-stranded RNA (dsRNA) and mount persistent stress response programs able to block tumor growth, even in highly immunosuppressed backgrounds. The dsRNA mimic polyinosine-polycytidylic acid, coadministered with polyethyleneimine as carrier, was identified as an unanticipated inducer of autophagy downstream of an exacerbated endosomal maturation program. A concurrent activity of the dsRNA helicase MDA-5 driving the proapoptotic protein NOXA resulted in an efficient autodigestion of melanoma cells. These results reveal tractable links for therapeutic intervention among dsRNA helicases, endo/lysosomes, and apoptotic factors. Cancer Cell . 2009 Aug 4;16(2):103-14. Cancer Cell 19647221 https://hdl.handle.net/20.500.12105/25498 TOLL-LIKE RECEPTORS POLYRIBOINOSINIC-POLYRIBOCYTIDYLIC ACID DOUBLE-STRANDED-RNA MALIGNANT-MELANOMA ER STRESS INTERFERON CANCER DEATH PROTEASOME MDA-5 Targeted activation of innate immunity for therapeutic induction of autophagy and apoptosis in melanoma cells.