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Cancer epigenetics

Dangerous unmarked genes

Nature Reviews Genetics volume 6, page 878 (2005)Cite this article

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They used conditional mutants of DNA methyltransferase to transiently remove methylation from mouse embryonic stem (ES) cells. When methylation was restored, imprinting patterns were lost — the maternal and paternal genomes were no longer differentially methylated. The authors derived fibroblasts from these ES cells and found that they were immortalized, grew at an increased rate and resisted inhibition by transforming growth factor β, a cytokine that inhibits the growth of various cell types.

Several tumour suppressors, such as Igf2r, Tsp1 and p57, were underexpressed in the fibroblasts, and oncogenes, such as Peg3, Peg5 and Igf2 were overexpressed. When the non-imprinted fibroblasts were injected into immunodeficient mice there was some tumorigenesis, compared with none in the controls. However, when the fibroblasts were also transfected with constitutively active Ras, tumorigenesis was much faster. The authors suggest that this is because Ras and LOI cooperate to form tumours.

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References

ORIGINAL RESEARCH PAPER

  1. Holm, T. M. et al. Global loss of imprinting leads to widespread tumorigenesis in adult mice. Cancer Cell 8, 275–285 (2005)

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FURTHER READING

  1. Robertson, K. D. DNA methylation and human disease. Nature Rev. Genet. 6, 597–610 (2005)

    Article  CAS  Google Scholar 

  2. Ushijima, T. Detection and interpretation of altered methylation patterns in cancer cells. Nature Rev. Cancer 5, 223–231 (2005)

    Article  CAS  Google Scholar 

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Authors
  1. Patrick Goymer
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Goymer, P. Dangerous unmarked genes. Nat Rev Genet 6, 878 (2005). https://doi.org/10.1038/nrg1759

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