Autophagy is a catabolic process whose activation may help cancer cells to adapt to cellular stress although, in some instances, it can induce cell death. Autophagy stimulation or inhibition has been considered an opportunity to treat cancer, especially in combination with anticancer therapies, although autophagy manipulation may be viewed as controversial. Thus, whether to induce or to inhibit autophagy may be the best option in the different cancer patients is still matter of debate. Her we will recapitulate the possible advantages or disadvantages of manipulating autophagy in cancer, not only with the aim to obtain cancer cell death and disable oncogenes, but also to evaluate its interplay with the immune response which is fundamental for the success of anticancer therapies. © 2019 The Author(s).

Autophagy manipulation as a strategy for efficient anticancer therapies: Possible consequences

D'Orazi, Gabriella
2019-01-01

Abstract

Autophagy is a catabolic process whose activation may help cancer cells to adapt to cellular stress although, in some instances, it can induce cell death. Autophagy stimulation or inhibition has been considered an opportunity to treat cancer, especially in combination with anticancer therapies, although autophagy manipulation may be viewed as controversial. Thus, whether to induce or to inhibit autophagy may be the best option in the different cancer patients is still matter of debate. Her we will recapitulate the possible advantages or disadvantages of manipulating autophagy in cancer, not only with the aim to obtain cancer cell death and disable oncogenes, but also to evaluate its interplay with the immune response which is fundamental for the success of anticancer therapies. © 2019 The Author(s).
2019
Autophagy
Cancer
Chloroquine (CQ)
Endoplasmic reticulum (ER stress)
HSF1
Hydroxichloroquine (HCQ)
Immunogenic cell death (ICD)
NRF2
p53
Unfolded protein response (UPR)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14245/11491
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