Reaching the point-of-no-return: the cornerstone of glioblastoma treatment?
The activation of cellular death programs does not necessarily predetermine an inevitable outcome. Identifying the precise moment when a cell irreversibly transitions from life to death presents a significant challenge in its assessment and measurement. In this review, we explore the critical altera...
| Autores: | , , |
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| Formato: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2025 |
| País: | España |
| Recursos: | Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya) |
| Repositorio: | Recercat. Dipósit de la Recerca de Catalunya |
| OAI Identifier: | oai:recercat.cat:2445/223515 |
| Acesso em linha: | https://hdl.handle.net/2445/223515 http://hdl.handle.net/2445/223515 |
| Access Level: | acceso abierto |
| Palavra-chave: | Mort cel·lular Regulació cel·lular Cell death Cellular control mechanisms |
| Resumo: | The activation of cellular death programs does not necessarily predetermine an inevitable outcome. Identifying the precise moment when a cell irreversibly transitions from life to death presents a significant challenge in its assessment and measurement. In this review, we explore the critical alterations in cellular structures that have been proposed as the point-of-no-return. Using glioblastoma as a model-one of the most aggressive and lethal tumor types with a remarkable ability to evade cell death-we highlight the challenge of reaching the point-of-no-return. Glioblastoma cells often exhibit impaired function of the apoptotic endonuclease, DFF40/CAD/CPAN, leading to incomplete apoptosis and genomic instability. The sublethal activation of DFF40/CAD/CPAN not only allows tumor cells to survive but can also drive more aggressive phenotypes and enhance therapeutic resistance. We underscore the need to reassess glioblastoma treatment strategies from broad cytotoxic approaches to more targeted therapies that exploit specific vulnerabilities within regulated cell death (RCD) pathways. |
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