MicroRNA-204 increases sensitivity of neuroblastoma cells to cisplatin and is associated with a favourable clinical outcome

Br J Cancer. 2012 Sep 4;107(6):967-76. doi: 10.1038/bjc.2012.356. Epub 2012 Aug 14.

Abstract

Background: Neuroblastoma remains a major cause of cancer-linked mortality in children. miR-204 has been used in microRNA expression signatures predictive of neuroblastoma patient survival. The aim of this study was to explore the independent association of miR-204 with survival in a neuroblastoma cohort, and to investigate the phenotypic effects mediated by miR-204 expression in neuroblastoma.

Methods: Neuroblastoma cell lines were transiently transfected with miR-204 mimics and assessed for cell viability using MTS assays. Apoptosis levels in cell lines were evaluated by FACS analysis of Annexin V-/propidium iodide-stained cells transfected with miR-204 mimics and treated with chemotherapy drug or vehicle control. Potential targets of miR-204 were validated using luciferase reporter assays.

Results: miR-204 expression in primary neuroblastoma tumours was predictive of patient event-free and overall survival, independent of established known risk factors. Ectopic miR-204 expression significantly increased sensitivity to cisplatin and etoposide in vitro. miR-204 direct targeting of the 3' UTR of BCL2 and NTRK2 (TrkB) was confirmed.

Conclusion: miR-204 is a novel predictor of outcome in neuroblastoma, functioning, at least in part, through increasing sensitivity to cisplatin by direct targeting and downregulation of anti-apoptotic BCL2. miR-204 also targets full-length NTRK2, a potent oncogene involved with chemotherapy drug resistance in neuroblastoma.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Apoptosis / genetics
  • Cell Line, Tumor
  • Cell Survival / genetics
  • Cisplatin / pharmacology*
  • Disease Models, Animal
  • Disease-Free Survival
  • Down-Regulation / drug effects
  • Drug Resistance, Neoplasm* / drug effects
  • Drug Resistance, Neoplasm* / genetics
  • Etoposide / pharmacology
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Kaplan-Meier Estimate
  • Membrane Glycoproteins / drug effects
  • Membrane Glycoproteins / metabolism
  • Mice
  • Mice, Inbred Strains
  • Mice, SCID
  • MicroRNAs / pharmacology*
  • Neuroblastoma / drug therapy*
  • Neuroblastoma / genetics*
  • Neuroblastoma / mortality
  • Predictive Value of Tests
  • Proportional Hazards Models
  • Protein-Tyrosine Kinases / drug effects
  • Protein-Tyrosine Kinases / genetics
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins / drug effects*
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2
  • Real-Time Polymerase Chain Reaction
  • Receptor, trkB / drug effects*
  • Receptor, trkB / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Up-Regulation

Substances

  • Antineoplastic Agents
  • MIRN204 microRNA, human
  • Membrane Glycoproteins
  • MicroRNAs
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Bcl2 protein, mouse
  • Etoposide
  • Ntrk2 protein, mouse
  • Protein-Tyrosine Kinases
  • Receptor, trkB
  • Cisplatin