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Atypical E2Fs inhibit tumor angiogenesis

B G M W Weijts1,2, B Westendorp1, B T Hien1

  • 1Department of Pathobiology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.

Oncogene
|September 20, 2017
PubMed

Insights

Atypical E2F transcription factors (E2F7 and E2F8) suppress tumor angiogenesis, a key cancer hallmark. This contrasts with their role in fetal development, revealing a novel tumor suppressor mechanism involving DLL4 regulation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Developmental Biology

Background:

  • Atypical E2F transcription factors (E2F7 and E2F8) are crucial for cell cycle regulation.
  • Inactivation of E2F7/8 leads to spontaneous cancer in mice, but their tumor suppressor mechanisms are unclear.

Purpose of the Study:

  • To investigate the role of atypical E2Fs in tumor angiogenesis.
  • To elucidate the mechanism by which E2F7/8 function as tumor suppressors.

Main Methods:

  • Genetic inactivation of E2F7/8 in epithelial and mesenchymal neoplasms.
  • Analysis of blood vessel formation in three distinct cancer models (chemical induction and oncogene overexpression).
  • Real-time imaging of blood vessel development in zebrafish xenografts.

Main Results:

  • Atypical E2Fs suppressed tumor angiogenesis across all three cancer models.
  • E2F7/8 deficiency led to enhanced intratumoral blood vessel branching in zebrafish xenografts.
  • DLL4 expression, a negative regulator of vascular branching, was decreased in E2F7/8-deficient tumors.

Conclusions:

  • Atypical E2Fs (E2F7/8) act as suppressors of tumor angiogenesis, a novel function distinct from their role in fetal development.
  • E2F7/8 may inhibit intratumoral vessel branching through the induction of DLL4.

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