| Full text | |
| Author(s): Show less - |
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]
Total Authors: 12
|
| Affiliation: | [1] Univ Fed Sao Paulo UNIFESP, Dept Farmacol, Escola Paulista Med, BR-04044020 Sao Paulo - Brazil
Total Affiliations: 1
|
| Document type: | Review article |
| Source: | Chemico-Biological Interactions; v. 206, n. 2, p. 279-288, NOV 25 2013. |
| Web of Science Citations: | 26 |
| Abstract | |
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) | |
| FAPESP's process: | 12/51215-4 - Autophagy and glycogen synthase kinase-3 (GSK3) as molecular targets capable of increasing the activity of drugs used in the treatment of myeloid leukemias (acute and chronic) |
| Grantee: | Claudia Bincoletto Trindade |
| Support type: | Regular Research Grants |