Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2017 Apr 28;49(4):e322.
doi: 10.1038/emm.2017.10.

DNA methylation: an epigenetic mark of cellular memory

Mirang Kim  1   2 , Joseph Costello  3
Affiliations
Review

DNA methylation: an epigenetic mark of cellular memory

Mirang Kim et al. Exp Mol Med. .

Abstract

DNA methylation is a stable epigenetic mark that can be inherited through multiple cell divisions. During development and cell differentiation, DNA methylation is dynamic, but some DNA methylation patterns may be retained as a form of epigenetic memory. DNA methylation profiles can be useful for the lineage classification and quality control of stem cells such as embryonic stem cells, induced pluripotent cells and mesenchymal stem cells. During cancer initiation and progression, genome-wide and gene-specific DNA methylation changes occur as a consequence of mutated or deregulated chromatin regulators. Early aberrant DNA methylation states occurring during transformation appear to be retained during tumor evolution. Similarly, DNA methylation differences among different regions of a tumor reflect the history of cancer cells and their response to the tumor microenvironment. Therefore, DNA methylation can be a useful molecular marker for cancer diagnosis and drug treatment.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
A model of epigenetic memory in iPSCs (modified from Ohi et al.). Induced pluripotent stem cells (iPSCs) harbor residual DNA methylation signatures from their donor cells. During reprogramming, pluripotency genes are demethylated and reactivated. Incomplete demethylation occurs in developmental regulators that are silenced in the somatic cell. Somatic cell genes were differentially methylated and repressed in iPSCs. Black, white and gray circles represent methylated, unmethylated and partially methylated CpGs, respectively.
Figure 2
Figure 2
A model of epigenetic memory in cancer cells. Cancers evolve by an iterative process of clonal expansion, genetic and epigenetic diversification and clonal selection within adaptive microenvironments. DNA methylation can be retained as an epigenetic memory of tumor evolution. Vertical line represents cancer treatments such as chemotherapy and radiation therapy. Small circles filled with black, white and gray represent DNA methylation pattern.
See this image and copyright information in PMC

References

    1. Bernstein BE, Meissner A, Lander ES. The mammalian epigenome. Cell 2007; 128: 669–681. - PubMed
    1. Bird A. DNA methylation patterns and epigenetic memory. Genes Dev 2002; 16: 6–21. - PubMed
    1. Hemberger M, Dean W, Reik W. Epigenetic dynamics of stem cells and cell lineage commitment: digging Waddington’s canal. Nat Rev Mol Cell Biol 2009; 10: 526–537. - PubMed
    1. Shipony Z, Mukamel Z, Cohen NM, Landan G, Chomsky E, Zeliger SR et al. Dynamic and static maintenance of epigenetic memory in pluripotent and somatic cells. Nature 2014; 513: 115–119. - PubMed
    1. Halley-Stott RP, Gurdon JB. Epigenetic memory in the context of nuclear reprogramming and cancer. Brief Funct Genomics 2013; 12: 164–173. - PMC - PubMed

Publication types