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SMYD3 Promotes Homologous Recombination via Regulation of H3K4-mediated Gene Expression

Yun-Ju Chen1, Cheng-Hui Tsai1, Pin-Yu Wang1

  • 1Department of Microbiology, College of Medicine, National Taiwan University, Taipei, 10051, Taiwan.

Scientific Reports
|June 21, 2017
PubMed

Insights

SMYD3, a cancer-promoting methyltransferase, also enhances DNA repair by stimulating homologous recombination gene transcription. Its deficiency impairs DNA repair and genome integrity in cancer cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • SMYD3 (SET and MYND domain-containing protein 3) is a methyltransferase frequently overexpressed in various cancers.
  • It typically acts as an oncogene, promoting cell cycle progression, proliferation, and metastasis.

Purpose of the Study:

  • To investigate the role of SMYD3 in DNA repair mechanisms, specifically homologous recombination (HR).
  • To elucidate the molecular mechanisms by which SMYD3 influences HR gene expression.

Main Methods:

  • Assessing DNA-damage sensitivity and homologous recombination repair foci in SMYD3-deficient cells.
  • Analyzing the transcriptional regulation of HR-related genes by SMYD3.
  • Investigating the role of H3K4 methylation at target gene promoters.

Main Results:

  • SMYD3 deficiency leads to hypersensitivity to DNA damage and impaired homologous recombination.
  • SMYD3 stimulates the transcription of genes crucial for multiple steps of homologous recombination.
  • SMYD3 regulates HR gene expression through H3K4 methylation at their promoter regions.

Conclusions:

  • SMYD3 plays a critical role in maintaining genome integrity in cancer by supporting homologous recombination.
  • Beyond its oncogenic functions, SMYD3 is essential for ensuring adequate expression of HR proteins to manage replication stress in cancer cells.

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