E2F1 activates p53 transcription through its distal site and participates in apoptosis induction in HPV-positive cells.

Abstract

The p53 tumor suppressor protein, one of the most extensively studied proteins, plays a pivotal role in cellular checkpoints that respond to DNA damage to prevent tumorigenesis. However, the transcriptional control of the p53 gene has not been fully characterized. We report that the transcription factor E2F1 binds only to the E2F1 distal site of the p53 promoter in the human papillomavirus positive carcinoma HeLa cell line. Moreover, we showed that etoposide, a DNA damaging agent, activates p53 transcription through the E2F1 pathway. This increase correlates with apoptosis induction as disruption of this pathway led to reduced apoptosis stimulation by the DNA damaging agent.

• Authors: Anthony Massip, Tania Arcondéguy, Christian Touriol, Céline Basset, Hervé Prats, Eric Lacazette
• Journal: FEBS letters (FEBS Lett) Vol. 587 Issue 19 Pg. 3188-94 (Oct 01 2013) ISSN: 1873-3468 [Electronic] England
• PMID: 23954287 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Chemical References

• DNA Primers
• E2F1 Transcription Factor
• E2F1 protein, human
• Etoposide

Topics

• Apoptosis (physiology)
• Base Sequence
• DNA Damage
• DNA Primers
• E2F1 Transcription Factor (physiology)
• Etoposide (pharmacology)
• Genes, p53
• HeLa Cells
• Humans
• Papillomaviridae (isolation & purification)
• Promoter Regions, Genetic
• Transcription, Genetic (drug effects, physiology)