Lung cancers are frequently characterized by inappropriate activation of epidermal growth factor receptor (EGFR)-dependent signaling and epigenetic silencing of the NADPH oxidase (NOX) enzyme DUOX1, both potentially contributing to worse prognosis.
Epigenetic silencing of NADPH oxidases by hypermethylation of their promoter region or of the genes required for their assembly and activity occurs in diseases, such as lung cancer, and may represent an early stage of neoplastic transformation.
Here we report that the NADPH oxidases DUOX1 and DUOX2, which are one of the main sources for reactive oxygen species production in the airway, are frequently silenced in human lung cancer.