The DOI matches its Crossref record; 64 of the 64 references it cites were found in a registry or an index.
Inhibition of autophagy increases susceptibility of glioblastoma stem cells to temozolomide by igniting ferroptosis
Open accessAbstract
The role of autophagy in cancer onset and progression appears still controversial. On one hand, autophagy allows cancer cell to survive in unfavorable environmental conditions, on the other hand, once internal energy resources are exhausted, it leads to cell death. In addition, autophagy interpheres with cell cycle progression, de facto exerting a cytostatic activity. Hence, it represents an important target for anticancer therapy. For example, temozolomide (TMZ), of use for glioblastoma (GBM) treatment, appears as capable of inducing autophagy partially inhibiting cancer cell proliferation. However, GBM, a very aggressive brain tumor with poor prognosis even after surgery and radio-chemotherapy, invariably recurs and leads to patient death. Since cancer stem cells have been hypothesized to play a role in refractory/relapsing cancers, in the present work we investigated if autophagy could represent a constitutive cytoprotection mechanism for glioblastoma stem-like cells (GSCs) and if the modulation of autophagic process could affect GBM growth and survival. Thus, in the present study we first evaluated the relevance of autophagy in GBM tumor specimens, then its occurrence in GSCs and, finally, if modulation of autophagy could influence GSC response to TMZ. Our results suggested that, in vitro, the impairing autophagic process with quinacrine, a compound able to cross the blood-brain barrier, increased GSC susceptibility to TMZ. Death of GSCs was apparently due to the iron dependent form of programmed cell death characterized by the accumulation of lipid peroxides called ferroptosis. These results underscore the relevance of the modulation of autophagy in the GSC survival and death and suggest that triggering of ferroptosis in GSCs could represent a novel and important target for the management of glioblastoma.
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Cites
1 retracted
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Cited by
Molecular mechanisms of ferroptosis and its role in cancer therapy
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Overcoming cancer chemotherapy resistance by the induction of ferroptosis
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Metadata
- Authors
- Buccarelli, M., Marconi, M., Pacioni, S., De Pascalis, I., D’Alessandris, Q. G., Martini, M., Ascione, B., Malorni, W., Larocca, L. M., Pallini, R., Ricci-Vitiani, L., & Matarrese, P.
- Venue
- Cell Death & Disease
- Published
- 2018-08-06
- Volume
- 9
- Issue
- 8
- Pages
- 841-841
- ISSN
- 2041-4889 (ISSN-L)
- OpenAlex
- W2886062107
- Cited by
- 257
- References
- 64
- FWCI
- 19.09
- Type
- journal article
- Language
- en
- Open access
- gold
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- Buccarelli, M., Marconi, M., Pacioni, S., De Pascalis, I., D’Alessandris, Q. G., Martini, M., Ascione, B., Malorni, W., Larocca, L. M., Pallini, R., Ricci-Vitiani, L., & Matarrese, P. (2018). Inhibition of autophagy increases susceptibility of glioblastoma stem cells to temozolomide by igniting ferroptosis. Cell Death & Disease. https://doi.org/10.1038/s41419-018-0864-7
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