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Oncogenic Biogenesis of pri-miR-17∼92 Reveals Hierarchy and Competition among Polycistronic MicroRNAs

Ariel O Donayo1, Radia M Johnson2, Hsin-Wei Tseng1

  • 1Department of Biochemistry, McGill University, 3655 Promenade Sir William Osler, Montreal, QC H3G 1Y6, Canada; Goodman Cancer Research Centre, McGill University, 1160 Pine Avenue W, Montreal, QC H3A 1A3, Canada.

Molecular Cell
|June 30, 2019
PubMed

Insights

Overexpressed microRNAs (miRNAs) in cancer disrupt their own processing. This leads to the downregulation of other tumor-suppressive miRNAs, contributing to cancer gene regulation.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Gene Regulation

Background:

  • The miR-17∼92 polycistron is frequently overexpressed in various cancers, driving oncogenic functions.
  • MicroRNAs (miRNAs) are key regulators of gene expression, and their dysregulation is a hallmark of cancer.

Purpose of the Study:

  • To elucidate the mechanism by which miR-17∼92 contributes to oncogenesis through disruption of miRNA processing.
  • To investigate the impact of miR-17∼92 overexpression on the processing of other endogenous miRNAs.

Main Methods:

  • Analysis of microprocessor complex association with pri-miR-17∼92 transcripts.
  • Characterization of miRNA processing intermediates.
  • Assessment of miRNA expression levels following oncogenic miR-17∼92 overexpression.

Main Results:

  • Oncogenic overexpression of miR-17∼92 leads to aberrant accumulation of partially processed intermediates.
  • These intermediates sequester the microprocessor complex, impairing the processing of other polycistronic miRNAs.
  • Selective downregulation of tumor-suppressive miRNAs, including miR-34b/c and Dlk1-Dio3 miRNAs, was observed.

Conclusions:

  • miR-17∼92 biogenesis intermediates disrupt endogenous miRNA processing, contributing to oncogenic rewiring of gene regulatory networks.
  • This mechanism reveals a novel functional paradigm for polycistronic miRNAs in cancer development.
Keywords:
13q31DGCR8Dlk1-Dio3DroshaEμ myc lymphomamiR-17∼92miR-19microRNAmicroRNA polycistronmicroprocessorprimary miRNA transcript

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