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Induction of Apoptosis in Human Oral Squamous Carcinoma Cells by Extracellular Products from Pseudomonas aeruginosa / 대한해부학회지
Korean Journal of Anatomy ; : 337-344, 2005.
Artículo en Inglés | WPRIM | ID: wpr-647025
ABSTRACT
It was reported that cancer in humans and animals infected with microbial pathogens was regressed about 100 years ago. Bacteria are able to trigger apoptosis by a variety of mechanisms including the secretion of protein synthesis inhibitors, pore forming proteins, molecules activating the endogenous death machinery in the infected cell. This study was conducted in order to investigate whether extracellular products of Psuedomonas aeruginosa (EPPA) induce apoptosis in human oral carcinoma cells (OSC9). The EPPA showed cytotoxic effect on OSC9 cells in dose and time-dependent manner. The cell death was demonstrated to be due to apoptosis characterized by chromatin condensation and nuclear fragment. EPPA treatment induced cleavage of caspase-3 and caspase-6. The caspase substrates, PARP, DFF45 and lamin A were cleaved during EPPA-induced apoptosis. Taken together, EPPA induces apoptosis on human oral squamous carcinoma cells in caspase-dependent manner. Our data therefore provide that EPPA contains a novel antitumor agent for human oral squamous carcinoma.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Pseudomonas / Pseudomonas aeruginosa / Bacterias / Inhibidores de la Síntesis de la Proteína / Cromatina / Carcinoma de Células Escamosas / Muerte Celular / Apoptosis / Lamina Tipo A / Caspasa 3 Límite: Animales / Humanos Idioma: Inglés Revista: Korean Journal of Anatomy Año: 2005 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Pseudomonas / Pseudomonas aeruginosa / Bacterias / Inhibidores de la Síntesis de la Proteína / Cromatina / Carcinoma de Células Escamosas / Muerte Celular / Apoptosis / Lamina Tipo A / Caspasa 3 Límite: Animales / Humanos Idioma: Inglés Revista: Korean Journal of Anatomy Año: 2005 Tipo del documento: Artículo