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Adenoviral E1A function through Myc

Abhishek A Chakraborty1, William P Tansey

  • 1Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.

Cancer Research
|January 2, 2009
PubMed

Insights

Adenovirus E1A protein stabilizes c-Myc by interacting with p400, activating oncogenic gene expression. This reveals E1A hijacks both E2F and c-Myc transcriptional networks for cancer development.

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • DNA tumor viruses, like adenovirus, provide insights into cancer-causing cellular pathways.
  • Adenovirus E1A oncoprotein is a key viral factor modulating host cell proteins, including retinoblastoma (Rb) and p400.
  • While E1A's interaction with Rb and E2F transcription factors is established, its downstream targets via p400 interaction were unclear.

Purpose of the Study:

  • To elucidate the downstream targets of the adenovirus E1A oncoprotein's interaction with the p400 chromatin remodeling protein.
  • To understand how E1A utilizes the c-Myc oncoprotein in oncogenesis.

Main Methods:

  • Investigated the interaction between adenovirus E1A, p400, and c-Myc.
  • Analyzed the formation of c-Myc-p400 complexes on chromatin.
  • Assessed the impact on c-Myc target gene activation.

Main Results:

  • Identified c-Myc as a critical downstream link in the E1A-p400 interaction.
  • Demonstrated that E1A binding to p400 stabilizes c-Myc.
  • Showed E1A promotes the formation of c-Myc-p400 complexes on chromatin, activating c-Myc target genes.

Conclusions:

  • The p400 chromatin remodeler plays a significant role in c-Myc function.
  • Adenovirus E1A promotes oncogenesis by co-opting the transcriptional networks of both E2F and c-Myc.

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