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The atypical E2F family member E2F7 couples the p53 and RB pathways during cellular senescence

Ozlem Aksoy1, Agustin Chicas, Tianying Zeng

  • 1Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.

Genes & Development
|July 18, 2012
PubMed

Insights

E2F7 is upregulated during oncogene-induced senescence, acting with RB and p53 to halt cell division and prevent cancer. This study reveals E2F7

Area of Science:

  • Cellular senescence
  • Cancer biology
  • Molecular oncology

Background:

  • Oncogene-induced senescence is a crucial anti-cancer mechanism.
  • This process is regulated by the retinoblastoma protein (RB) and p53 pathways.

Purpose of the Study:

  • To investigate the role of E2F transcription factors in oncogene-induced senescence.
  • To elucidate the relationship between E2F7, RB, and p53 in cellular anti-cancer responses.

Main Methods:

  • Analysis of E2F family member expression during senescence.
  • Investigating E2F7's transcriptional activity and target genes.
  • Studying the interplay between E2F7, RB, and p53 in cell cycle control.

Main Results:

  • E2F7 is the sole E2F transcription factor significantly upregulated during oncogene-induced senescence.
  • E2F7 acts as a direct p53 transcriptional target, repressing E2F target genes.
  • E2F7 cooperates with RB to enforce cell cycle arrest and compensates for RB loss to prevent proliferation.

Conclusions:

  • E2F7 plays a critical role in cellular senescence and tumor suppression.
  • A novel functional link between the RB and p53 pathways involving E2F7 is uncovered.

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