miR-143 Interferes with ERK5 Signaling, and Abrogates Prostate Cancer Progression in Mice

Cyrielle Clape*, Vanessa Fritz, Corinne Henriquet, Florence Apparailly, Pedro Luis Fernandez, Francois Iborra, Christophe Avances, Martin Villalba, Stephane Culine, Lluis Fajas

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

173 Citations (Scopus)

Abstract

Background: Micro RNAs are small, non-coding, single-stranded RNAs that negatively regulate gene expression at the post-transcriptional level. Since miR-143 was found to be down-regulated in prostate cancer cells, we wanted to analyze its expression in human prostate cancer, and test the ability of miR-43 to arrest prostate cancer cell growth in vitro and in vivo.

Results: Expression of miR-143 was analyzed in human prostate cancers by quantitative PCR, and by in situ hybridization. miR-143 was introduced in cancer cells in vivo by electroporation. Bioinformatics analysis and luciferase-based assays were used to determine miR-143 targets. We show in this study that miR-143 levels are inversely correlated with advanced stages of prostate cancer. Rescue of miR-143 expression in cancer cells results in the arrest of cell proliferation and the abrogation of tumor growth in mice. Furthermore, we show that the effects of miR-143 are mediated, at least in part by the inhibition of extracellular signal-regulated kinase-5 (ERK5) activity. We show here that ERK5 is a miR-143 target in prostate cancer.

Conclusions: miR-143 is as a new target for prostate cancer treatment.

Original languageEnglish
Article number7542
Number of pages8
JournalPLoS One
Volume4
Issue number10
DOIs
Publication statusPublished - 26 Oct 2009

Keywords

  • ACTIVATED-RECEPTOR-GAMMA
  • MICRORNA EXPRESSION
  • PROMOTES ADIPOGENESIS
  • RADICAL PROSTATECTOMY
  • INVASION
  • PATHWAY
  • AND-145
  • GROWTH
  • TUMORS
  • RISK

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