Abstract
Lung cancer is the most common form of malignant neoplasia and is one of the leading causes of cancer death. According to the World Health Organization (WHO), radon is the second leading cause of lung cancer after smoking. Exposure to radon leads to the death of cells of the bronchial epithelium of the lungs, which is accompanied by the release of a large amount of mitochondrial DNA. Free-circulating mitochondrial DNA (fc mtDNA) can serve as a kind of trigger for the transduction of pro-inflammatory signals in animal cells. The production of fc mtDNA can occur as a result of apoptosis processes. Any ionizing radiation, including alpha radiation, to which radon belongs, promotes the promotion of cell death both as a result of direct mechanical action on the cell due to reactive oxygen species (ROS), and due to the appearance of unrepairable damage to the genetic material. In addition, radon can alter the expression profile of miRNAs, which in turn can activate apoptosis and inflammation. Free-circulating mitochondrial DNA by activating the Nf-kb signaling pathway mediates the synthesis of proinflammatory cytokines, and as a result of this activation, inflammation develops, which is one of the key factors in lung cancer oncogenesis. This short review analyzes the molecular mechanisms of lung cancer associated with the carcinogenic effect of radon based on the analysis of the fc mtDNA level, the profile of the tissue-specific microRNA fraction, the level and spectrum of pro- and anti-inflammatory cytokines.