Aberrant methylation is one of the driving forces of
cancer genome development. Although the rate of methylation appears massively variable across the genome, it is mainly observed in
histone modification,
chromatin organization,
DNA accessibility, or promoter sequence. Methylation of promoter sequence occurs mostly to
cytosine nucleotides, which can affect
transcription factors' binding affinities. In this study, we demonstrated that
cytosine repeats (C types density), consisting of CC, CCC, CCCC, CCCCC, CCCCCC, CCCCCCC motifs and CpG islands density in 25 proto-oncogenes, tumor suppressor genes and control genes may play a role in the pathogenesis of
acute myeloid leukemia. The promoter sequences were divided into a 100
nucleotide window from -500 to +100
nucleotides and 20
nucleotide window from -100 to +100. Each window is analyzed to find the higher C type and CpG islands density, which may cause the increased methylation in the promoter sequence. Our novel findings show that promoter sequence
cytosine repeats and CpG density increase closer to transcription sites, especially just before and after the transcription start site (TSS). The results demonstrate that
cytosine density increases while proto-oncogenes and TSG promoter sequences are closer to TSS 50.8% and 41.0% respectively, if (-500 to -200) and (-100 to +100) windows of the nucleotide sequences are compared. This proves that around TSS location has special nucleotide motifs and could be an important implication for our understanding of potential methylating locations in promoters.