Our results address a number of central questions about the temporal relationship between gene expression, DNA hypermethylation, and chromatin modification in cancer cells. In this study, we now demonstrate that the seeds of DNA methylation also play an important role in initiating chromatin modification.
We previously reported that hypermethylation of the GSTP1 CpG island promoter in prostate cancer cells is initiated by a combination of transcriptional gene silencing (by removal of the Sp1 sites) and seeds of methylation that, instead of being constantly removed because of demethylation associated with transcription, acts as a catalyst for the spread of methylation across the CpG island.
Glutathione S-transferase ( GSTP1) is one example of a gene that is hypermethylated and inactivated in the majority of prostate cancers.
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