The class of highly bioactive chemicals known as reactive oxygen species (ROS) has been extensively explored in relation to several malignancies and is thought to be a typical by-product of many cellular functions. Cancer cells have greater baseline ROS concentrations than healthy cells because of an imbalance between oxidants and antioxidants. At low to moderate levels, ROS functions as a signal transducer to drive cell proliferation, migration, invasion, and angiogenesis. ROS also has a second role in cellular metabolism. On the other hand, excessive ROS may kill cells by harming organelles, membranes, lipids, proteins, and nucleic acids. Numerous studies have shown that anticancer treatments that regulate ROS levels, such as immunotherapy, provide encouraging outcomes both in vitro and in vivo.
The tumor microenvironment (TME) is a field with a high ROS concentration made up of many distinct cell types, including cancer cells, cancer-associated fibroblasts, and many immune cells. One of the key reasons for immunotherapy resistance in the TME is a high quantity of ROS (including immune checkpoint blockade). However, it would be foolish to just eliminate ROS since they often play several functions and because the beneficial/unfavorable switch may be readily changed by changing the ROS concentration, location, species, and environment in which they are present. For instance, ROS may raise the expression of PD-L1, but it is not viable to remove PD-L1 by depleting ROS since doing so would significantly reduce the immunostimulatory effects of ROS and have unfavorable consequences related to redox imbalance. Overall, the link between ROS and cancer immunity is still unclear, highlighting the need for further research to increase the effectiveness of immunotherapies.
In this Research Topic, the submission of both Original Research and Review articles are welcome, including but not limited to the following subtopics:
? Molecular mechanism of ROS production in cancer cells;
? Cell death induced by ROS;
? The crosstalk between ROS and immune cells;
? Interwoven effects of ROS in cancer immunotherapy.
Please NOTE: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
The class of highly bioactive chemicals known as reactive oxygen species (ROS) has been extensively explored in relation to several malignancies and is thought to be a typical by-product of many cellular functions. Cancer cells have greater baseline ROS concentrations than healthy cells because of an imbalance between oxidants and antioxidants. At low to moderate levels, ROS functions as a signal transducer to drive cell proliferation, migration, invasion, and angiogenesis. ROS also has a second role in cellular metabolism. On the other hand, excessive ROS may kill cells by harming organelles, membranes, lipids, proteins, and nucleic acids. Numerous studies have shown that anticancer treatments that regulate ROS levels, such as immunotherapy, provide encouraging outcomes both in vitro and in vivo.
The tumor microenvironment (TME) is a field with a high ROS concentration made up of many distinct cell types, including cancer cells, cancer-associated fibroblasts, and many immune cells. One of the key reasons for immunotherapy resistance in the TME is a high quantity of ROS (including immune checkpoint blockade). However, it would be foolish to just eliminate ROS since they often play several functions and because the beneficial/unfavorable switch may be readily changed by changing the ROS concentration, location, species, and environment in which they are present. For instance, ROS may raise the expression of PD-L1, but it is not viable to remove PD-L1 by depleting ROS since doing so would significantly reduce the immunostimulatory effects of ROS and have unfavorable consequences related to redox imbalance. Overall, the link between ROS and cancer immunity is still unclear, highlighting the need for further research to increase the effectiveness of immunotherapies.
In this Research Topic, the submission of both Original Research and Review articles are welcome, including but not limited to the following subtopics:
? Molecular mechanism of ROS production in cancer cells;
? Cell death induced by ROS;
? The crosstalk between ROS and immune cells;
? Interwoven effects of ROS in cancer immunotherapy.
Please NOTE: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
