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Multiple mechanisms disrupt the let-7 microRNA family in neuroblastoma

John T Powers1, Kaloyan M Tsanov1, Daniel S Pearson1

  • 1Division of Pediatric Hematology/Oncology, Boston Children's Hospital, Boston, Massachusetts 02115, USA.

Nature
|July 8, 2016
PubMed

Insights

LIN28B is dispensable in neuroblastoma, as high MYCN RNA levels sponge tumor-suppressing let-7 microRNAs. let-7 disruption, through various mechanisms, drives neuroblastoma development and poor prognosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Neuroblastoma prognosis is linked to MYCN amplification.
  • MYCN is targeted by let-7 tumor suppressor microRNAs.
  • LIN28B inhibits let-7 biogenesis and is overexpressed in neuroblastoma.

Purpose of the Study:

  • Investigate the role of LIN28B in MYCN-amplified neuroblastoma.
  • Clarify the relationship between LIN28B, MYCN, and let-7.
  • Determine the impact of let-7 disruption on neuroblastoma pathogenesis.

Main Methods:

  • Analysis of MYCN-amplified neuroblastoma cell lines.
  • Assessment of let-7 microRNA levels and activity.
  • Correlation of genetic alterations with clinical outcomes.

Main Results:

  • LIN28B is dispensable in MYCN-amplified neuroblastoma despite let-7 de-repression.
  • High MYCN messenger RNA levels effectively sponge let-7.
  • Genetic loss of let-7 is common, inversely associated with MYCN amplification, and linked to poor prognosis.

Conclusions:

  • let-7 disruption, via LIN28B, MYCN sponging, or genetic loss, is a unifying mechanism in neuroblastoma.
  • These findings have broad implications for understanding cancer pathogenesis.

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