Investigation of the Effect of Decitabine on Hep-2 Cell Line at Chromosomal Level

Abstract

DNA methylation is an epigenetic event that is defined as the binding of a methyl group via DNA methyl transferases (DNMTs) to the fifth carbon of cytosine in the CpG dinucleotide. Regulation of the expressions of tissue-specific genes, regulation of gene expressions during development, X inactivation and imprinting events are caused by DNA methylation. The aberrant DNA methylation associated with various diseases, especially cancers, is one of the most studied epigenetic mechanisms. Decitabine, a nucleoside analogue, inhibits DNMT enzymes and causes hypomethylation in the genome. There are many studies investigating the aberrant DNA methylation status in the genome of cells treated with Decitabine. Karyotype analysis is a cytogenetic method, which has been used successfully for the detection of both numerical and structural chromosomal abnormalities for many years. Hep-2 is a laryngeal cancer cell line, which is, used to investigate various genetic and epigenetic changes at the molecular level that revealed important information about the initiation and development of laryngeal cancer. However, the number of studies showing the chromosomal structure of Hep-2 cells is insufficient. The effects of Decitabine on cell morphology in different cell lines, its relationship with proliferation of the cells and its effects on chromosomes have been studied. However, the number of studies showing the effect of Decitabine at the chromosomal level in Hep-2 cell lines is also very limited. In current study, we investigated the chromosomes of Hep-2 cells cultured 72 hours with 1 μM and 10 μM Decitabine and without Decitabine.

Keywords: Cell lines, Hep-2 cell line, Karyotyping, Decitabine, DNA methylation

DOI: 10.7176/JSTR/5-4-11