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Redox signaling: Potential arbitrator of autophagy and apoptosis in therapeutic response
Lu Zhang1, Kui Wang2, Yunlong Lei3
1State 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.
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.
Insights
Reactive oxygen species (ROS) act as crucial signals in cancer therapy, regulating cell death and survival pathways like autophagy and apoptosis. Understanding this redox signaling is key to developing new cancer treatments.
Area of Science:
- Cell Biology
- Biochemistry
- Oncology
Background:
- Redox signaling, involving reactive oxygen species (ROS), is critical for cell death and survival during cancer therapy.
- Autophagy and apoptosis are distinct cellular processes that respond to stress, including oxidative stress, to control cell fate.
- While high ROS levels damage cells, lower levels act as signaling molecules regulating autophagy and apoptosis.
Purpose of the Study:
- To elucidate the molecular mechanisms by which redox signaling orchestrates autophagy and apoptosis.
- To explore the cross-talk between ROS-regulated autophagy and apoptosis.
- To discuss the therapeutic implications of understanding redox signaling in cancer treatment.
Main Methods:
- Literature review and synthesis of current research on redox signaling, autophagy, and apoptosis.
- Analysis of molecular pathways involved in ROS-mediated cell fate determination.
- Discussion of potential strategies for cancer treatment based on redox signaling modulation.
Main Results:
- Basic ROS levels function as signaling molecules promoting cell survival and proliferation.
- Increased ROS levels can trigger both autophagy and apoptosis by damaging cellular components.
- ROS-regulated autophagy and apoptosis exhibit cross-talk, influencing overall cell fate.
Conclusions:
- Redox signaling delicately controls cell fate by orchestrating autophagy and apoptosis.
- A deeper understanding of these mechanisms can lead to novel cancer therapeutic strategies.
- Targeting ROS-mediated pathways offers potential for improved cancer treatment outcomes.
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