ROS-mediated mechanisms of autophagy stimulation and their relevance in cancer therapy.
Mounting evidence suggests that reactive oxygen species (ROS) are multifaceted signaling molecules implicated in a variety of cellular programs during physiological as well as pathological conditions. Recently, ROS produced endogenously, by deranged metabolism of cancer cells, or exogenously, by ROS-generating drugs, have been shown to promote macroautophagy, a lysosomal pathway of self-degradation with essential prosurvival functions. Several molecular aspects of the modulation of autophagy pathways by ROS have been revealed in the past years and it is now clear that these processes are mutually linked and play a crucial role in cancer progression and in response to cancer therapeutics. In this review we address the molecular mechanisms underlying the activation of autophagy pathways by ROS and focus on the role of autophagy in cancer cells responding to ROS-producing agents, which are utilized as a therapeutic modality to kill cancer cells.
Dewaele
Michael
M
Cell Death Research and Therapy Laboratory, Department of Molecular Cell Biology, Faculty of Medicine, Katholieke Universiteit Leuven, Belgium.
Maes
Hannelore
H
Agostinis
Patrizia
P
D000970:Antineoplastic Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000502:physiology; D001343:Autophagy / Q000502:physiology*; D002986:Clinical Trials as Topic; D006801:Humans; D009369:Neoplasms / Q000628:therapy*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology; D010778:Photochemotherapy; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology
D000970:Antineoplastic Agents; D017382:Reactive Oxygen Species