Article ID Journal Published Year Pages File Type
10769813 Biochemical and Biophysical Research Communications 2005 9 Pages PDF
Abstract
The overexpression of DNA polymerase β (β-pol) has been identified in lots of human cancers, but the mechanism has seldom been investigated. Telomerase transcriptional element-interacting factor (TEIF) can bind to hTERT promoter, stimulating its transcription and telomerase activities. Here, we report that TEIF could also enhance the expression of β-pol at transcription level. TEIF could specifically activate transcription of β-pol promoter, but not that of DNA polymerase α or δ promoter. The responsible sequences for binding of TEIF were revealed as GC-rich elements dispersing from +19 to −29 nt of β-pol promoter, which due to mutations caused decreasing in binding of TEIF and apparent losing of transactivation activity. The in vivo interaction between TEIF and β-pol promoter was identified by chromatin immunoprecipitation assay. Besides, ectopic expression of TEIF in HeLa cells could upregulate both levels of endogenous β-pol mRNA and protein, and consequently increases resistance to the oxidative stress of H2O2. The data may provide new clue to the elucidation of β-pol overexpression in cancers and also a functional link between β-pol and telomerase.
Related Topics
Life Sciences Biochemistry, Genetics and Molecular Biology Biochemistry
Authors
, , , , ,