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Cyclin D1 induction of Dicer governs microRNA processing and expression in breast cancer

Zuoren Yu1, Liping Wang, Chenguang Wang

  • 11] Department of Cancer Biology, Thomas Jefferson University, 233 South 10th Street, Philadelphia, Pennsylvania 19107, USA [2] Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, Pennsylvania 19107, USA [3] Research Center for Translational Medicine, Key Laboratory for Basic Research in Cardiology, East Hospital, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China.

Nature Communications
|November 30, 2013
PubMed

Insights

Cyclin D1 regulates microRNA processing by inducing Dicer expression, a key enzyme for gene silencing. This coordination is crucial for cell cycle progression and is linked to breast cancer subtypes.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Cyclin D1 is a cell cycle regulator promoting proliferation and oncogenesis.
  • Dicer is essential for microRNA (miRNA) maturation and gene silencing.
  • The interplay between cell cycle control and the non-coding genome is not well understood.

Purpose of the Study:

  • To investigate the mechanism by which the cell cycle, specifically Cyclin D1, influences microRNA processing.
  • To determine if Cyclin D1 directly impacts Dicer expression and function.
  • To explore the functional consequences of the Cyclin D1-Dicer interaction in cell proliferation and cancer.

Main Methods:

  • Analysis of cyclin D1 knockout cells and rescue experiments.
  • In vitro and in vivo studies assessing Dicer expression.
  • Investigation of the transcriptional regulation of Dicer by Cyclin D1.
  • Correlation analysis of Cyclin D1 and Dicer expression in human breast cancer subtypes.
  • Assessment of heterochromatic histone modifications and cell migration assays.

Main Results:

  • Cyclin D1 knockout cells exhibit defects in pre-microRNA processing, which are rescued by Cyclin D1.
  • Cyclin D1 directly induces Dicer expression through a cdk-independent transcriptional mechanism.
  • Cyclin D1 and Dicer expression are significantly correlated in luminal A and basal-like breast cancer.
  • Both proteins maintain heterochromatic histone modifications (Tri-m-H3K9).
  • Cyclin D1-driven cell proliferation and migration are dependent on Dicer activity.

Conclusions:

  • Cyclin D1 plays a critical role in coordinating microRNA biogenesis through the induction of Dicer.
  • This regulatory axis is important for cell cycle progression, heterochromatin maintenance, and potentially oncogenesis.
  • The findings highlight a direct link between cell cycle machinery and the regulation of the non-coding genome.

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