NOX2-Derived Reactive Oxygen Species in Cancer.
Hanna Grauers WiktorinEbru AydinKristoffer HellstrandAnna MartnerPublished in: Oxidative medicine and cellular longevity (2020)
The formation of reactive oxygen species (ROS) by the myeloid cell NADPH oxidase NOX2 is critical for the destruction of engulfed microorganisms. However, recent studies imply that ROS, formed by NOX2+ myeloid cells in the malignant microenvironment, exert multiple actions of relevance to the growth and spread of neoplastic cells. By generating ROS, tumor-infiltrating myeloid cells and NOX2+ leukemic myeloid cells may thus (i) compromise the function and viability of adjacent cytotoxic lymphocytes, including natural killer (NK) cells and T cells, (ii) oxidize DNA to trigger cancer-promoting somatic mutations, and (iii) affect the redox balance in cancer cells to control their proliferation and survival. Here, we discuss the impact of NOX2-derived ROS for tumorigenesis, tumor progression, regulation of antitumor immunity, and metastasis. We propose that NOX2 may be a targetable immune checkpoint in cancer.
Keyphrases
- reactive oxygen species
- induced apoptosis
- cell cycle arrest
- cell death
- dendritic cells
- papillary thyroid
- acute myeloid leukemia
- endoplasmic reticulum stress
- bone marrow
- oxidative stress
- dna damage
- squamous cell carcinoma
- stem cells
- nk cells
- signaling pathway
- squamous cell
- cell proliferation
- immune response
- gene expression
- pi k akt