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Updated: Aug 9, 2025

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The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies

Yu Zhu1, Zi Wang1, Yanan Li1

  • 1Department of Hematology, The Second Xiangya Hospital, Molecular Biology Research Center, School of Life Sciences, Hunan Province Key Laboratory of Basic and Applied Hematology, Central South University, Changsha 410011, China.

Cancers
|February 25, 2023
PubMed

Insights

Disordered histone acetylation, driven by CREB-binding protein (CREBBP) and E1A-binding protein P300 (EP300), promotes blood cancers. Targeting these key proteins offers new therapeutic strategies for hematological malignancies.

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • Disordered histone acetylation is a hallmark of hematological malignancies.
  • CREB-binding protein (CREBBP) and E1A-binding protein P300 (EP300) are crucial acetyltransferases regulating gene expression.
  • Dysregulation of CREBBP/EP300 contributes to cancer initiation, progression, and chemoresistance.

Purpose of the Study:

  • To review the role of CREBBP/EP300 in normal hematopoiesis.
  • To elucidate the pathogenic mechanisms of CREBBP/EP300 in hematological malignancies.
  • To discuss therapeutic implications of targeting CREBBP/EP300.

Main Methods:

  • Literature review of CREBBP/EP300 functions in hematology.
  • Analysis of CREBBP/EP300 involvement in hematological malignancies.
  • Exploration of therapeutic strategies targeting CREBBP/EP300.

Main Results:

  • CREBBP/EP300 are vital for normal blood cell development.
  • CREBBP/EP300 dysregulation drives hematological cancers and influences immune responses.
  • These proteins are critical for chemoresistance in blood cancers.

Conclusions:

  • CREBBP/EP300 play significant roles in both physiological and pathological hematological processes.
  • Targeting CREBBP/EP300 presents promising therapeutic avenues for hematological malignancies.
  • Further research into CREBBP/EP300 inhibitors is warranted for clinical application.

Keywords:
CREBBPEP300acetylationchemoresistancehematological malignancyimmunotherapy

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