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 (AU)