title: Redox signaling: Potential arbitrator of autophagy and apoptosis in therapeutic response.
abstract: Redox signaling plays important roles in the regulation of cell death and survival in response to cancer therapy. Autophagy and apoptosis are discrete cellular processes mediated by distinct groups of regulatory and executioner molecules, and both are thought to be cellular responses to various stress conditions including oxidative stress, therefore controlling cell fate. Basic levels of reactive oxygen species (ROS) may function as signals to promote cell proliferation and survival, whereas increase of ROS can induce autophagy and apoptosis by damaging cellular components. Growing evidence in recent years argues for ROS that below detrimental levels acting as intracellular signal transducers that regulate autophagy and apoptosis. ROS-regulated autophagy and apoptosis can cross-talk with each other. However, how redox signaling determines different cell fates by regulating autophagy and apoptosis remains unclear. In this review, we will focus on understanding the delicate molecular mechanism by which autophagy and apoptosis are finely orchestrated by redox signaling and discuss how this understanding can be used to develop strategies for the treatment of cancer.
authors.affiliation: State Key Laboratory for Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center of Biotherapy, Chengdu, 610041, P.R. China; Department of Neurology, the Affiliated Hospital of Hainan Medical College, Haikou, 570102, P.R. China.
authors.forename: Lu
authors.initials: L
authors.lastname: Zhang
authors.affiliation: State Key Laboratory for Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center of Biotherapy, Chengdu, 610041, P.R. China.
authors.forename: Kui
authors.initials: K
authors.lastname: Wang
authors.affiliation: Department of Biochemistry and Molecular Biology, and Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, P.R. China.
authors.forename: Yunlong
authors.initials: Y
authors.lastname: Lei
authors.affiliation: Department of Neurology, the Affiliated Hospital of Hainan Medical College, Haikou, 570102, P.R. China.
authors.forename: Qifu
authors.initials: Q
authors.lastname: Li
authors.affiliation: Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria 3800, Australia.
authors.forename: Edouard Collins
authors.initials: EC
authors.lastname: Nice
authors.affiliation: State Key Laboratory for Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center of Biotherapy, Chengdu, 610041, P.R. China. Electronic address: hcanhua@hotmail.com.
authors.forename: Canhua
authors.initials: C
authors.lastname: Huang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001343:Autophagy / Q000502:physiology*; D006801:Humans; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
keywords: Apoptosis; Autophagy; Cancer therapy; ROS; Redox signaling