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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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SETD1A modulates cell cycle progression through a miRNA network that regulates p53 target genes

Ken Tajima1, Toshifumi Yae1, Sarah Javaid1

  • 1Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts 02129, USA.

Nature Communications
|September 24, 2015
PubMed

Insights

The histone methyltransferase SETD1A suppresses the cancer gene BTG2 indirectly via microRNAs, impacting cell cycle and tumor growth. This reveals a novel mechanism for gene silencing in cancer.

Area of Science:

  • Cancer Biology
  • Epigenetics
  • Gene Regulation

Background:

  • The antiproliferative gene BTG2 is often downregulated in cancers without direct mutations.
  • Alternative gene silencing mechanisms for BTG2 are suggested.
  • Histone lysine methyltransferases (KMTs) are implicated in cancer development.

Purpose of the Study:

  • To identify the mechanism suppressing BTG2 expression in cancer.
  • To investigate the role of KMTs in regulating BTG2.
  • To understand how chromatin regulators impact cancer-related genes.

Main Methods:

  • shRNA screen targeting 43 histone lysine methyltransferases (KMTs).
  • Analysis of miRNA induction and gene expression.
  • In vitro cell cycle assays.
  • Mouse xenograft models for tumorigenesis studies.

Main Results:

  • SETD1A was identified as a suppressor of BTG2 expression.
  • SETD1A induces BTG2-targeting microRNAs (miRNAs), leading to gene downregulation.
  • This indirect miRNA-dependent mechanism affects multiple p53 pathway genes.
  • SETD1A regulates cell cycle progression and modulates tumorigenesis in vivo.

Conclusions:

  • SETD1A suppresses BTG2 via an indirect miRNA-dependent mechanism.
  • This pathway explains specific genetic consequences of chromatin modulator alterations in cancer.
  • Findings elucidate a novel epigenetic regulation of tumor suppressor genes.

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