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A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation

Zuoren Yu1, Chenguang Wang, Min Wang

  • 1Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.

The Journal of Cell Biology
|August 13, 2008
PubMed

Insights

MicroRNAs (miRNAs) like miR-17/20 suppress tumors by inhibiting cyclin D1. This study reveals a feedback loop where cyclin D1 promotes miR-17/20, which then limits cell proliferation in breast cancer.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • MicroRNAs (miRNAs) are implicated in tumor suppression due to decreased expression in human cancers.
  • The miR-17-5p/miR-20a miRNA cluster's role in breast cancer pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the regulatory relationship between the miR-17-5p/miR-20a miRNA cluster and cyclin D1 in breast cancer.
  • To determine the functional impact of this interaction on cell proliferation and oncogenesis.

Main Methods:

  • Correlation analysis of miRNA and cyclin D1 levels in human breast tumors and cell lines.
  • Functional assays assessing the effects of miR-17/20 on cell proliferation, colony formation, and cell cycle progression.
  • Experiments using cyclin D1 siRNA and cyclin D1-deficient cells to validate miRNA-mediated effects.
  • In vivo studies and promoter analysis to explore the feedback loop mechanism.

Main Results:

  • Inverse correlation observed between miR-17-5p/miR-20a levels and cyclin D1 abundance in breast cancer.
  • miR-17/20 suppressed breast cancer cell proliferation and colony formation by inhibiting cyclin D1 translation.
  • The cell cycle inhibitory effects of miR-17/20 were dependent on cyclin D1 expression.
  • Cyclin D1 was found to induce miR-17-5p and miR-20a expression and bind to their promoter region.

Conclusions:

  • A novel regulatory feedback loop exists between cyclin D1 and the miR-17/20 miRNA cluster in breast cancer.
  • Cyclin D1 induces miR-17/20 expression, which in turn suppresses cyclin D1's proliferative function.
  • This interaction links miRNA cluster expression to the regulation of breast cancer oncogenesis.

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