New Insight into the Role of AhR in Lung Carcinogenesis

Abstract Lung cancer (LC), one of the most common malignant neoplasms, is the leading cause of high cancer mortality worldwide. Smoking is a risk factor for almost all histological types of LC. Benzo[ a ]pyrene (BaP), one of the main constituents of tobacco smoke, can cause cancer. It has been established that its toxic effects can develop in the following ways: genotoxic (formation of adducts with DNA) and non-genotoxic or epigenetic. The latter is less known, although it is known that BaP activates aryl hydrocarbon receptor (AhR), which regulate transcription of many target genes, including microRNAs, which can lead to initiation and enhancement of the malignant cell transformation. Recent studies are evaluating the role of AhR in the regulation of immune checkpoints, as cigarette smoke and BaP induce the AhR-regulated expression of PD-L1 ( CD274 ) in lung epithelial cells in vitro and in vivo . In ad