Abstract
DNA methylation is one of the most important epigenetic modifications next to acetylation or histone modifications, as it has a role in the homeostatic control of the cell and is strongly involved in the control of genome expression. DNA methylation, which is catalyzed by DNA methyltransferases (DNMTs), is one of the primary epigenetic mechanisms that control cell proliferation, apoptosis, differentiation, cell cycle, and transformation in eukaryotes. Hypomethylation and hypermethylation result in the activation or repression of genes and in a normal cell there is a strict balance between these processes. Abnormal DNA methylation is a well-known feature of cancer development and progression and can turn normal stem cells into cancer stem cells. Studies clearly show that DNA methylation regulates gene transcription functions in cancer pathogenesis. In cancer cells, DNA methylation patterns are largely modified, and therefore, methylation is used to distinguish cancer cells from normal, healthy cells. However, the mechanisms underlying changes in DNA methylation remain unexplored. However, it is known that oxidative stress (OS) is a key mechanism of carcinogenesis, and DNA methylation of genes that are active at OS may play a role in cancer development. Studies also show that DNA methylation is mediated by long noncoding RNA (lncRNA) under both physiological and pathological conditions. How cell-specific DNA methylation patterns are established or disrupted is a key question in developmental biology and cancer epigenetics.