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Multifaceted role of redox pattern in the tumor immune microenvironment regarding autophagy and apoptosis
Yuqing Ren1,2, Ruizhi Wang1, Siyuan Weng1
1Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Abstract:
The reversible oxidation-reduction homeostasis mechanism functions as a specific signal transduction system, eliciting related physiological responses. Disruptions to redox homeostasis can have negative consequences, including the potential for cancer development and progression, which are closely linked to a series of redox processes, such as adjustment of reactive oxygen species (ROS) levels and species, changes in antioxidant capacity, and differential effects of ROS on downstream cell fate and immune capacity. The tumor microenvironment (TME) exhibits a complex interplay between immunity and regulatory cell death, especially autophagy and apoptosis, which is crucially regulated by ROS. The present study aims to investigate the mechanism by which multi-source ROS affects apoptosis, autophagy, and the anti-tumor immune response in the TME and the mutual crosstalk between these three processes. Given the intricate role of ROS in controlling cell fate and immunity, we will further examine the relationship between traditional cancer therapy and ROS. It is worth noting that we will discuss some potential ROS-related treatment options for further future studies.
Insights
Disruptions in redox homeostasis, involving reactive oxygen species (ROS), are linked to cancer. This study explores how ROS impacts apoptosis, autophagy, and anti-tumor immunity within the tumor microenvironment.
Area of Science:
- Biochemistry
- Cell Biology
- Immunology
Background:
- Redox homeostasis is a critical signaling pathway influencing physiological responses.
- Imbalances in redox homeostasis, particularly reactive oxygen species (ROS) levels, are implicated in cancer development and progression.
- The tumor microenvironment (TME) involves complex interactions between immunity, cell death (apoptosis, autophagy), and ROS.
Purpose of the Study:
- To investigate the mechanisms by which multi-source ROS influences apoptosis, autophagy, and anti-tumor immunity in the TME.
- To elucidate the crosstalk between ROS, apoptosis, autophagy, and anti-tumor immune responses.
- To examine the relationship between conventional cancer therapies and ROS, and explore potential ROS-targeted treatments.
Main Methods:
- The study will analyze the role of ROS in regulating apoptosis and autophagy within the TME.
- Investigate the impact of ROS on anti-tumor immune responses.
- Examine the interplay between ROS, cell death pathways, and immune evasion in cancer.
Main Results:
- ROS levels and species significantly affect cell fate, immune capacity, and regulatory cell death (apoptosis and autophagy) in the TME.
- A complex crosstalk exists between ROS, apoptosis, autophagy, and anti-tumor immunity.
- ROS plays a crucial role in modulating the efficacy of traditional cancer therapies.
Conclusions:
- Understanding ROS-mediated regulation of apoptosis, autophagy, and immunity in the TME is vital for cancer therapy.
- ROS-targeted strategies hold promise for novel cancer treatment approaches.
- Further research into the intricate role of ROS in cancer is warranted.
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