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Nfkb na modulação redox do crescimento celular em câncer de pulmão de não-pequenas células

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Nfkb na modulação redox do crescimento celular em câncer de pulmão de não-pequenas células

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Título Nfkb na modulação redox do crescimento celular em câncer de pulmão de não-pequenas células
Autor Oliveira, Valeska Aguiar de
Orientador Klamt, Fabio
Co-orientador Motta, Leonardo Lisbôa da
Data 2011
Nível Graduação
Instituição Universidade Federal do Rio Grande do Sul. Faculdade de Farmácia. Curso de Farmácia.
Assunto Catalase
Neoplasias pulmonares
Tumores
[en] A549
[en] Catalase
[en] NSCLC
[en] Tumor aggressiveness
Abstract Lung cancer is the most lethal malignant disease worldwide with limited efficacy of current therapeutics and dismal prognostic. Approximately 80% of the cases are non-small cell lung cancer (NSCLC). NFB is a major transcription factor associated with tumor progression that responds to stressful stimuli, such as oxidative stress, influencing cell survival and chemoresistance. Since NSCLC aggressiveness is associated with higher intracellular oxidative stress, this study evaluated the involvement of NFB in the redox modulation of tumor aggressiveness in the human NSCLC cell line A549. Treatment with the antioxidant enzyme catalase (CAT) (1000 U/mL) for 96h inhibited cell proliferation and when the enzyme was withdraw of the enzyme restored cell proliferation rates. In addition, catalase treatment decreased intracellular thiol levels (SH) and non-enzymatic antioxidant potential (TRAP). This redox modulation could be explained by the antioxidant contribution provided by high dose of exogenous CAT and was also reverted when the enzyme was withdraw. In agreement with the decreases in antioxidant defenses, the activation of the redox-sensitive transcription factor NFB was decreased in catalase-treated cells as assessed by Western blotting for the nuclear content of the NFB member p65. Taken together, data presented here suggest that decreases in the pro-oxidant status of lung cancer cells with catalase treatment can inhibit cell proliferation and activation of tumor-associated signaling pathways, providing a new therapeutic strategy for NSCLC therapy.
Tipo Trabalho de conclusão de graduação
URI http://hdl.handle.net/10183/70122
Arquivos Descrição Formato
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