E2F1 and telomerase: alliance in the dark side

Cell Cycle. 2006 May;5(9):930-5. doi: 10.4161/cc.5.9.2698. Epub 2006 May 1.


Cancer arises from a stepwise accumulation of genetic changes. Among these changes, deregulation of the Rb/E2F1 pathway and constitutively active telomerase are pivotal milestones for the attainment of immortality and maintaining the neoplastic phenotype. We recently showed the Rb/E2F1 pathway to be a direct modulator of telomerase activity in normal and cancer cells, specifically in malignant gliomas. In addition, we reported that the correlation between the levels of expression of E2F1 and hTERT -the catalytic subunit of telomerase- in a subset of patients with glioblastoma multiforme confers clinical relevance to the role of E2F1 in triggering or maintaining hTERT expression. Here we review the evidence supporting the mechanistic linkage between E2F1 and telomerase activation. We also consider the clinical implications of this association in terms of prognostic significance and opportunities for the development of new and more rational therapeutic strategies.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Biomarkers, Tumor
  • DNA-Binding Proteins / metabolism*
  • E2F1 Transcription Factor / genetics
  • E2F1 Transcription Factor / physiology*
  • Enzyme Activation
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Models, Biological
  • Neoplasms / enzymology*
  • Neoplasms / genetics
  • Neoplasms / pathology
  • Telomerase / metabolism*


  • Biomarkers, Tumor
  • DNA-Binding Proteins
  • E2F1 Transcription Factor
  • E2F1 protein, human
  • Telomerase