Influence of overexpression of BCL-2 family proteins on pomolic acidtriggered apoptosis (2005)
- Authors:
- Autor USP: MENDES, JOAO GUSTAVO PESSINI AMARANTE - ICB
- Unidade: ICB
- Assunto: IMUNOLOGIA
- Language: Português
- Abstract: Objetivo: In previous studies we showed the Pomolic acid, a triterpene with anti-MDR activity, triggers apoptosis through the mitochondrial pathway. This pathway is initiated by alterations of the mitochondrial membrane potential, followed by release of apoptotic factors and activation of caspases leading to cell death. Members of the Bcl-2 family of proteins, such as Bcl-2 and Bcl-xL, play a pivotal role in the regulation of the mitochondrial-induced apoptosis pathway. As overexpression of Bcl-2 and Bcl-xL may lead to tumor cells resistance to chemotherapy, we asked whether they could also interfere with pomolic acid activity. The aim of this work was to evaluate the effect of Bcl-2 and Bcl-xL overexpression in pomolic acid-induced apoptosis of HL-60 (chronic myeloid leukemia) cells. Métodos e Resultados: For this investigation, HL-60 cells and their transfected derivatives HL-60-Bcl-2 and HL-60-Bcl-xL were used. Flow cytometry was used to determine DNA fragmentation and loss of mitochondrial membrane potential (_ _ m) in cells stained with Pi or DiOC6, respectively. Activation of caspases - 3, and -9 was analyzed by western blot. Overexpression of Bcl-2 and Bcl-xL partially inhibits pomolic acid-induced loss of mitochondrial membrane potential and subsequent apoptosis. This inhibition was higher on the HL-60 cells transfected with Bcl-xL. Activation of caspase -3 and -9 was strongly inhibited in transfected cells. Conclusões: Overexpression of theanti-apoptotic genes Bcl-2 and Bcl-xL. modulated the anti-tumoral activity of pomolic acid. The decrease in PA-induced loss of mitochondrial potential in cells transfected with Bcl-2 and Bcl-xL, corroborates the proposed hypothesis of mitochondria as the target for pomolic acid activity. However in spite of the down modulation of apoptosis caused by the overexpression of these proteins, the strong anti-tumoral activity of PA is still preserved
- Imprenta:
- Publisher: Federação de Sociedades de Biologia Experimental
- Publisher place: Águas de Lindóia, São Paulo
- Date published: 2005
- Source:
- Título do periódico: Resumos
- Conference titles: Reunião Anual da Federação de Sociedades de Biologia Experimental, FeSBE
-
ABNT
FERNANDES, J. et al. Influence of overexpression of BCL-2 family proteins on pomolic acidtriggered apoptosis. 2005, Anais.. Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental, 2005. . Acesso em: 24 abr. 2024. -
APA
Fernandes, J., Weinlich, R., Castilho, R. O., Amarante-Mendes, J. G. P., & Gattass, C. R. (2005). Influence of overexpression of BCL-2 family proteins on pomolic acidtriggered apoptosis. In Resumos. Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental. -
NLM
Fernandes J, Weinlich R, Castilho RO, Amarante-Mendes JGP, Gattass CR. Influence of overexpression of BCL-2 family proteins on pomolic acidtriggered apoptosis. Resumos. 2005 ;[citado 2024 abr. 24 ] -
Vancouver
Fernandes J, Weinlich R, Castilho RO, Amarante-Mendes JGP, Gattass CR. Influence of overexpression of BCL-2 family proteins on pomolic acidtriggered apoptosis. Resumos. 2005 ;[citado 2024 abr. 24 ] - Modulation of fasl and activation-induced cell death (aicd) of do11.10 T-cells hybridoma by imiquimod
- Aumento de galectina-I mediado por BCR-ABL contribuiu para a transformação maligna na leucemia mielóide crônica
- Apoptosis: a programme of cell death or cell disposal?
- Therapeutic applications of TRAIL receptor agonists in cancer and beyond
- Calpain functions in a caspase-independent manner to promote apoptosis-like events during platelet activation
- Transcriptional changes induced by the BCR-ABL inhibitor STI571 in an in vitro experimental model of chronic myelogenous leukemia
- Apoptose: programa molecular de morte celular
- Butyrate increases apoptosis induced by different antineoplastic drugs in monocytic leukemia cells
- The point of no return: mitochondria, caspases, and the commitment to cell death
- Bcl-2-independent Bcr-Abl-mediated resistance to apoptosis: protection is correlated with up regulation of Bcl-'X IND. L'
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
