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. Author manuscript; available in PMC: 2008 Jun 23.
Published in final edited form as: J Cell Biochem. 2008 Feb 1;103(2):509–519. doi: 10.1002/jcb.21417

Fig. 6.

Fig. 6

Proposed mechanism of epigenetic gene control alterations by EGCG. A: Under normal growth conditions DNMT1 methylation capacity is not inhibited allowing methylation of the hTERT promoter in cancer cells which may block the binding of the Rb/E2F-1/DNMT1/HDAC1 repressor complex, the results of which include a hypermethylated promoter, acetylated histones and active gene transcription. B: Treatment of EGCG inhibits DNMT1 methylating ability leading to hypomethylation of the hTERT promoter [Fang et al., 2003] including key E2F-1 sites. This may allow the Rb/E2F-1/HDAC1 repressor complex to bind leading to hypoacetylation and reduced hTERT transcription. [Color figure can be viewed in the online issue, which is available at www.interscience.wiley.com.]