Role of Hypoxia-Mediated Autophagy in Tumor Cell Death and Survival

Programmed cell death or type I apoptosis has been extensively studied and its contribution to the pathogenesis of disease is well established. However, autophagy functions together with apoptosis to determine the overall fate of the cell. The cross talk between this active self-destruction process...

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Bibliographic Details
Published in:Cancers 2021-01, Vol.13 (3), p.533
Main Authors: Zaarour, Rania F, Azakir, Bilal, Hajam, Edries Y, Nawafleh, Husam, Zeinelabdin, Nagwa A, Engelsen, Agnete S T, Thiery, Jérome, Jamora, Colin, Chouaib, Salem
Format: Article
Language:English
Subjects:
Apoptosis
Autophagy
Cancer
Cancer immunotherapy
Cell death
Cell growth
Cell proliferation
Cell survival
Chemotherapy
Genes
Glucose
Homeostasis
Hypoxia
Immune response
Kinases
Phagocytosis
Phosphorylation
Proteins
Review
Transcription factors
Tumor cells
Tumor suppression
Tumorigenesis
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Summary:Programmed cell death or type I apoptosis has been extensively studied and its contribution to the pathogenesis of disease is well established. However, autophagy functions together with apoptosis to determine the overall fate of the cell. The cross talk between this active self-destruction process and apoptosis is quite complex and contradictory as well, but it is unquestionably decisive for cell survival or cell death. Autophagy can promote tumor suppression but also tumor growth by inducing cancer-cell development and proliferation. In this review, we will discuss how autophagy reprograms tumor cells in the context of tumor hypoxic stress. We will illustrate how autophagy acts as both a suppressor and a driver of tumorigenesis through tuning survival in a context dependent manner. We also shed light on the relationship between autophagy and immune response in this complex regulation. A better understanding of the autophagy mechanisms and pathways will undoubtedly ameliorate the design of therapeutics aimed at targeting autophagy for future cancer immunotherapies.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers13030533