As the largest cause of cancer-related deaths worldwide, pulmonary cancer is the most common form of the disease. Several genetic, epigenetic, and environmental factors come into play during the multi-step mechanism of tumorigenesis. The heterogeneity that makes discovering successful therapeutics for pulmonary cancer problematic is significantly influenced by the epigenetic landscape, including DNA methylation, chromatin architecture, histone modifications, and noncoding RNA control. Clinical activity of epigenetic-targeted medicines has been reported in hematological tumors, and these compounds may also have therapeutic effects in solid tumors. Over the course of the past few years, some researchers have successfully modified the expression of genes in cells using the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas (CRISPR-associated proteins) technique. The utilization of this technology allows for the induction of site-specific mutagenesis, epigenetic alterations, and the regulation of gene expression. This study will present an overview of the primary epigenetic alterations seen in pulmonary cancer, as well as a summary of therapeutic implications for targeting epigenetics in the management of pulmonary cancer, with a particular emphasis on the technique known as CRISPR/Cas9.
Keywords: CRISPR; Cancer therapy; Epigenetic; NSCLC; SCLC.
© 2022. The Author(s), under exclusive licence to Federación de Sociedades Españolas de Oncología (FESEO).