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Hypermethylation of the hTERT promoter inhibits the expression of telomerase activity in normal oral fibroblasts and senescent normal oral keratinocytes
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Hypermethylation of the hTERT promoter inhibits the expression of telomerase activity in normal oral fibroblasts and senescent normal oral keratinocytes
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Hypermethylation of the hTERT promoter inhibits the expression of telomerase activity in normal oral fibroblasts and senescent normal oral keratinocytes
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Journal Article
Hypermethylation of the hTERT promoter inhibits the expression of telomerase activity in normal oral fibroblasts and senescent normal oral keratinocytes
2003
Overview
Telomerase activity in human cells closely correlates with the expression of its catalytic subunit, telomerase reverse transcriptase (
hTERT
). Previously, we reported the lack of telomerase activity in normal human oral fibroblasts (NHOF) and the diminution of telomerase activity during senescence in normal human oral keratinocytes (NHOK). To investigate the underlying mechanisms of telomerase regulation in both cell types, we analysed the expression, promoter activity, and methylation status of the
hTERT
gene. The expression of
hTERT
mRNA diminished in senescent NHOK, but was not detected in NHOF at any stage of replication. An exogenous
hTERT
promoter was active in NHOF and in senescing NHOK, indicating that the lack of
hTERT
gene expression resulted from alteration of the endogenous
hTERT
promoter. Since methylation is involved in the silencing of numerous genes, we carried out DNA methylation assays. The assay revealed that the
hTERT
promoter was hypermethylated in NHOF and was gradually methylated during senescence in NHOK. Treatment of NHOF and senescent NHOK with the demethylating agent 5-aza-2′-deoxycytidine restored the expression of endogenous
hTERT
mRNA. Our results suggest that hypermethylation of the
hTERT
promoter plays a critical role in the negative regulation of telomerase activity in normal human oral cells.
Publisher
Nature Publishing Group UK,Nature Publishing Group
