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.

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.

Related Concept Videos

Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
5.0K
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
6.1K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
3.2K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.3K
Redox Reactions01:27

Redox Reactions

Redox reactions are vital biochemical processes that underpin energy metabolism in cells. These reactions involve the transfer of electrons between molecules, occurring in tandem as oxidation and reduction. Oxidation refers to the loss of electrons, while reduction denotes their gain. This coupling ensures the seamless flow of electrons through metabolic pathways. For example, in bacterial metabolism, glucose undergoes oxidation to carbon dioxide, while oxygen is simultaneously reduced to...
1.4K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.9K