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Exploitation of EP300 and CREBBP Lysine Acetyltransferases by Cancer

Narsis Attar1,2, Siavash K Kurdistani1,2,3,4

  • 1Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, California 90095.

Cold Spring Harbor Perspectives in Medicine
|November 25, 2016
PubMed

Insights

p300 and CREB-binding protein (CBP) are crucial for cellular functions, including gene regulation and metabolism. Cancer cells exploit these proteins, with genetic alterations in p300/CBP contributing to various malignancies.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • p300 and CREB-binding protein (CBP) are homologous lysine acetyltransferases with diverse cellular roles.
  • These proteins function as transcriptional regulators and impact non-transcriptional processes like DNA replication and metabolism.
  • p300/CBP are frequently exploited by oncogenes and cancer cells to promote and sustain oncogenic phenotypes.

Purpose of the Study:

  • To discuss the multifaceted biological functions of p300/CBP.
  • To elucidate how cancer cells utilize p300/CBP for transformation and maintaining malignancy.
  • To review the contribution of p300/CBP alterations to the cancer phenotype.

Main Methods:

  • Literature review and synthesis of existing research on p300/CBP.
  • Analysis of genetic alterations (mutations, expression changes, localization) in p300 and CBP across various cancers.
  • Discussion of functional consequences of these alterations in the context of cancer biology.

Main Results:

  • p300/CBP possess extensive transcriptional and non-transcriptional roles critical for normal cellular function.
  • Cancer cells leverage p300/CBP activity for cellular transformation and oncogenesis.
  • Aberrant p300/CBP function, due to genetic alterations, is a common feature in both solid tumors and hematological malignancies, contributing to cancer development and progression.

Conclusions:

  • Disruption of p300/CBP biological functions through genetic alterations significantly contributes to the development and maintenance of cancer.
  • Understanding these mechanisms offers potential therapeutic targets for cancer treatment.
  • The context-dependent role of p300/CBP in cancer highlights the complexity of targeting these proteins.

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