Human Molecular Genetics, Vol 8, 459-470, Copyright © 1999 by Oxford University Press
TH Huang, MR Perry and DE Laux
CpG island hypermethylation is known to be associated with gene silencing
in cancer. This epigenetic event is generally accepted as a stochastic
process in tumor cells resulting from aberrant DNA methyltransferase
(DNA-MTase) activities. Specific patterns of CpG island methylation could
result from clonal selection of cells having growth advantages due to
silencing of associated tumor suppressor genes. Alternatively, methylation
patterns may be determined by other, as yet unidentified factors. To
explore further the underlying mechanisms, we developed a novel array-based
method, called differential methylation hybridization (DMH), which allows a
genome- wide screening of hypermethylated CpG islands in tumor cells. DMH
was used to determine the methylation status of >276 CpG island loci in
a group of breast cancer cell lines. Between 5 and 14% of these loci were
hypermethylated extensively in these cells relative to a normal control.
Pattern analysis of 30 positive loci by Southern hybridization indicated
that CpG islands might differ in their susceptibility to hypermethylation.
Loci exhibiting pre-existing methylation in normal controls were more
susceptible to de novo methylation in these cancer cells than loci without
this condition. In addition, these cell lines exhibited different intrinsic
abilities to methylate CpG islands not directly associated with
methyltransferase activities. Our study provides evidence that, aside from
random DNA-MTase action, additional cellular factors exist that govern
aberrant methylation in breast cancer cells.
ARTICLES
Methylation profiling of CpG islands in human breast cancer cells
Departments of Pathology and Anatomical Sciences, Ellis Fischel Cancer Center, University of Missouri, 115 Business Loop I-70 West, Columbia, MO 65203, USA. huangh@health.missouri.edu
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