The function of DNA methylation in lung cancer: Diagnostic and clinical implications

Currently, the detection of lung cancer depends on chest X-ray, low-dose computed tomography (CT) scans, and tissue biopsy. However, harmful radiation from X-rays and CT scans may increase cancer risk. In contrast, biopsy of the lungs is highly laborious and painful. These diagnostic limitations contribute to delayed diagnosis, and treatment is therefore less effective at advanced stages. DNA methylation is a mechanism in which DNA methyltransferases add a methyl group to the cytosine–phosphate–guanine islands of a gene, which can either enhance or suppress its expression. Previous research has shown that promoter methylation of protooncogenes and tumor suppressor genes begins at the early stages of tumorigenesis and can be detected in cell-free DNA derived from blood plasma. With this primary objective, we highlight DNA hypomethylation in proto-oncogenes and hypermethylation in tumor suppressor genes in lung cancer patients, which may serve as therapeutic targets for the development of treatments that may increase the survival rate of lung cancer patients.