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A Double-Negative Feedback Interaction between MicroRNA-29b and DNMT3A/3B Contributes to Ovarian Cancer Progression

Yue Teng1, Xiaohang Zuo, Meng Hou

  • 1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an Jiaotong University, Xi'an, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|November 11, 2016
PubMed
Abstract

Insights

This study reveals miR-29b regulates DNA methylation in ovarian cancer by targeting DNMT3A/3B. This epigenetic feedback loop offers potential for new miR-29b-based ovarian cancer therapies.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Epigenetic abnormalities are common in epithelial ovarian cancer (EOC).
  • Tumor-suppressor microRNAs (epi-miRNAs) can counteract these abnormalities.
  • miR-29b is a known epi-miRNA with potential roles in EOC.

Purpose of the Study:

  • To investigate the role of miR-29b in DNA methylation regulation in EOC cells.
  • To elucidate the relationship between miR-29b and DNA methyltransferases (DNMTs) in EOC.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR), western blotting, and immunohistochemistry assessed miR-29b and DNMT3A/3B expression.
  • Functional roles were tested using anti-miRs and microRNA precursors.
  • Luciferase reporter assays and Co-immunoprecipitation (Co-IP) investigated direct interactions.

Main Results:

  • miR-29b expression was inversely correlated with DNMT3A/3B levels in EOC.
  • miR-29b directly targeted DNMT3A/3B mRNAs, leading to their downregulation.
  • A double-negative feedback loop was identified: DNMT3A/3B modulated miR-29b expression via DNA methylation, and miR-29b regulated DNMT3A/3B.

Conclusions:

  • A novel epigenetic regulatory circuit involving miR-29b and DNMT3A/3B was uncovered in EOC.
  • This crosstalk suggests potential for miR-29b-based therapeutic strategies for EOC treatment.

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