Combined effects of radon exposure and TP53 knockout

Lung cancer is a multi-causal disease. Among the many pathogenic factors, radioactive radon and its progeny are considered to be the second risk factor for lung cancer after smoking, and it is also the first among never-smokers. Radon (Rn) is a colorless and odorless radioactive gas, which has been designated as a human carcinogen by the International Agency for Research on Cancer(IARC) and the U.S. Environmental Protection Agency. Long-term radon exposure can increase the incidence of lung cancer in non-smokers, which is usually related to mutations in the TP53 gene. The genetic variation of the tumor suppressor gene TP53 can promote the occurrence and development of human cancer in different ways, and it occurs in almost all types of cancer. Mitochondria are organelles of multiple catabolic and anabolic pathways necessary for the maintenance and proliferation of cells. Through a series of in vivo and in vitro experiments, we observe the effects of radon exposure and TP53 knockout on cells and mitochondria, and then screen and verify the mitochondrial-related genes targeted by TP53 through high-throughput sequencing and bio-informatics analysis, so as to provide new experimental evidence for clarifying the mechanism of radon-induced malignant transformation of lung cells.