| Texto completo | |
| Autor(es): Mostrar menos - |
Bincoletto, C.
[1]
;
Bechara, A.
[1]
;
Pereira, G. J. S.
[1]
;
Santos, C. P.
[1]
;
Antunes, F.
[1]
;
da-Silva, J. Peixoto
[1]
;
Muler, M.
[1]
;
Gigli, R. D.
[1]
;
Monteforte, P. T.
[1]
;
Hirata, H.
[1]
;
Jurkiewicz, A.
[1]
;
Smaili, S. S.
[1]
Número total de Autores: 12
|
| Afiliação do(s) autor(es): | [1] Univ Fed Sao Paulo UNIFESP, Dept Farmacol, Escola Paulista Med, BR-04044020 Sao Paulo - Brazil
Número total de Afiliações: 1
|
| Tipo de documento: | Artigo de Revisão |
| Fonte: | Chemico-Biological Interactions; v. 206, n. 2, p. 279-288, NOV 25 2013. |
| Citações Web of Science: | 26 |
| Resumo | |
Autophagy is a mechanism of protection against various forms of human diseases, such as cancer, in which autophagy seems to have an extremely complex role. In cancer, there is evidence that autophagy may be oncogenic in some contexts, whereas in others it clearly contributes to tumor suppression. In addition, studies have demonstrated the existence of a complex relationship between autophagy and cell death, determining whether a cell will live or die in response to anticancer therapies. Nevertheless, we still need to complete the autophagy-apoptosis puzzle in the tumor context to better address appropriate chemotherapy protocols with autophagy modulators. Generally, tumor cell resistance to anticancer induced-apoptosis can be overcome by autophagy inhibition. However, when an extensive autophagic stimulus is activated, autophagic cell death is observed. In this review, we discuss some details of autophagy and its relationship with tumor progression or suppression, as well as role of autophagy-apoptosis in cancer treatments. (C) 2013 Elsevier Ireland Ltd. All rights reserved. (AU) | |
| Processo FAPESP: | 12/51215-4 - Autofagia e glicogênio sintase quinase-3 (GSK3) como alvos moleculares capazes de aumentar a atividade de fármacos utilizados no tratamento de leucemias mielóides (aguda e crônica) |
| Beneficiário: | Claudia Bincoletto Trindade |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |