| pubmed-article:15963946 | pubmed:abstractText | The overexpression of DNA polymerase beta (beta-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 beta-pol at transcription level. TEIF could specifically activate transcription of beta-pol promoter, but not that of DNA polymerase alpha or delta promoter. The responsible sequences for binding of TEIF were revealed as GC-rich elements dispersing from +19 to -29 nt of beta-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 beta-pol promoter was identified by chromatin immunoprecipitation assay. Besides, ectopic expression of TEIF in HeLa cells could upregulate both levels of endogenous beta-pol mRNA and protein, and consequently increases resistance to the oxidative stress of H2O2. The data may provide new clue to the elucidation of beta-pol overexpression in cancers and also a functional link between beta-pol and telomerase. | lld:pubmed |
