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DNMT3b Modulates Melanoma Growth by Controlling Levels of mTORC2 Component RICTOR

Goran Micevic1, Viswanathan Muthusamy2, William Damsky3

  • 1Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA.

Cell Reports
|March 1, 2016
PubMed

Insights

DNA methyltransferase DNMT3B promotes melanoma by regulating miR-196b and mTORC2 signaling. DNMT3B inhibition may offer a new therapeutic strategy for melanoma treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • DNA methyltransferase DNMT3B is overexpressed in tumors, impacting cancer development.
  • DNMT3B's specific roles and signaling pathways in melanoma remain unclear.

Purpose of the Study:

  • Investigate DNMT3B's function in human melanoma.
  • Elucidate the molecular mechanisms by which DNMT3B influences melanoma progression.

Main Methods:

  • Utilized a Braf/Pten mouse melanoma model to assess the impact of DNMT3B loss.
  • Analyzed DNA methylation, miR-196b expression, and mTORC2 pathway activation.

Main Results:

  • DNMT3B loss significantly suppressed melanoma formation in mice.
  • DNMT3B deficiency led to miR-196b promoter hypomethylation and increased miR-196b expression.
  • miR-196b directly targeted Rictor, inhibiting mTORC2 activation and subsequent melanoma growth.

Conclusions:

  • DNMT3B acts as a pro-tumorigenic factor in melanoma by controlling mTORC2 signaling via miR-196b.
  • DNMT3B represents a potential therapeutic target for melanoma treatment.

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