Related Experiment Video

Updated: May 9, 2025

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
09:58

Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis

Published on: June 27, 2020

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The oncoprotein DEK controls growth-regulated gene expression by enhancing the DNA-binding activity of basic leucine

Takuma Hashimoto1, Shoko Saito1,2, Mike Ohata2

  • 1Graduate School of Pharmaceutical Sciences, Kitasato University, Minato-ku, Japan.

The FEBS Journal
|May 3, 2025
PubMed

Insights

The oncogenic protein DEK promotes cancer by enhancing DNA binding of transcription factors. DEK knockdown reduced cancer cell growth and migration, suggesting DEK drives malignancy through these interactions.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Overexpression of the oncogenic protein DEK is linked to poor cancer prognosis.
  • The precise molecular mechanisms of DEK in cancer development are not fully understood.
  • DEK is known to interact with and enhance the activity of certain transcription factors.

Purpose of the Study:

  • To investigate the hypothesis that DEK promotes cancer cell phenotypes by regulating transcription factors.
  • To elucidate the molecular mechanisms underlying DEK's role in cancer progression.

Main Methods:

  • Analysis of DEK's interaction with basic leucine zipper (bZIP) and basic helix-loop-helix leucine zipper (bHLH-ZIP) transcription factors.
  • In vitro assessment of DEK's effect on transcription factor DNA-binding capacity.
  • DEK knockdown in lung adenocarcinoma A549 cells followed by global transcriptome analysis.

Main Results:

  • DEK binds to the basic regions of bZIP and bHLH-ZIP transcription factors.
  • DEK enhances the DNA-binding capacity of C/EBPα and ATF3 in vitro.
  • DEK knockdown decreased genes involved in cell growth and amino acid metabolism, potentially regulated by c-Jun and c-Myc.
  • DEK knockdown reduced A549 cell growth, colony formation, and migration.

Conclusions:

  • DEK promotes cancer cell malignancy by modulating the function of bZIP and bHLH-ZIP transcription factors.
  • DEK's interaction with transcription factors is a key mechanism driving cancer progression.
  • Targeting DEK-transcription factor interactions may offer therapeutic strategies for cancer treatment.
Keywords:
DEKRNA‐sequencebZIP transcription factorcancergene regulation

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