Molecular mechanisms of apoptosis induction by AICAR and the new prohibitin-binding compound fluorizoline
[eng] The pro-apoptotic effects of two new drugs have been studied for the development of new strategies for cancer treatment. On the one hand, we proved that AICAR induces apoptosis in an AMPK- and p53-independent manner in mouse embryonic fibroblasts. The analysis of the BCL-2 family members allow...
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| Formato: | tesis doctoral |
| Estado: | Versión publicada |
| Fecha de publicación: | 2015 |
| País: | España |
| Recursos: | Universidad de Barcelona |
| Repositorio: | Dipòsit Digital de la UB |
| OAI Identifier: | oai:diposit.ub.edu:2445/102861 |
| Acesso em linha: | https://hdl.handle.net/2445/102861 http://hdl.handle.net/10803/396235 |
| Access Level: | acceso abierto |
| Palavra-chave: | Càncer Apoptosi Cancer Apoptosis |
| Resumo: | [eng] The pro-apoptotic effects of two new drugs have been studied for the development of new strategies for cancer treatment. On the one hand, we proved that AICAR induces apoptosis in an AMPK- and p53-independent manner in mouse embryonic fibroblasts. The analysis of the BCL-2 family members allowed the identification of the BH3-only proteins BIM and NOXA as required for apoptosis induction by AICAR. In addition, we characterized the mechanism of action of fluorizoline (compound 1a), a new drug that specifically binds to prohibitin 1 and 2. The presence of prohibitins was proved to be essential for the pro-apoptotic effects of fluorizoline. Prohibitins mediate the increases in BIM and NOXA, two proteins that play a key role in the onset of apoptosis by fluorizoline. |
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