AI Article Synopsis
- The regulation of the hTERT gene is important for cell transformation and differentiation, and the E2 protein from human papillomavirus (HPV) plays a role in inhibiting cell growth and inducing cell death in infected cells.
- The study found that E2 represses the hTERT promoter by interacting with the Sp1 transcription factor, while not affecting E-Box-mediated transcription.
- Additionally, experiments showed that E2 is directly recruited to the hTERT promoter, shedding light on its function in HPV-related cellular processes.
Article Abstract
The transcriptional regulation of the human telomerase reverse transcriptase (hTERT) gene is a critical step in transformation and differentiation. Human papillomavirus E2 protein inhibits cell growth in HPV-infected cells and triggers apoptosis in HeLa cells. Because E2 induces cell growth suppression and senescence, we hypothesize that the protein may modulate cellular gene expression related to these processes. In this report, we demonstrate that E2 inhibits the hTERT promoter. The mapping of the E2-responsive region of hTERT reveals that Sp1 is important for E2-mediated repression of this promoter in 293T cells. Site-directed mutagenesis data on the hTERT promoter show that E2 does not abolish E-Box-mediated transcription and represses promoter activity via the Sp1 binding site. Furthermore, chromatin immunoprecipitation assays indicate that E2 is actively recruited to the hTERT promoter region. Our findings provide novel insights into the biological function of human papillomavirus E2.
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| http://dx.doi.org/10.1074/jbc.M203706200 | DOI Listing |
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