MiR-200c is a cMyc-activated miRNA that promotes nasopharyngeal carcinoma by downregulating PTEN

Oncotarget. 2017 Jan 17;8(3):5206-5218. doi: 10.18632/oncotarget.14123.

Abstract

The c-Myc transcription factor regulates a complex transcriptional program that leads to cellular transformation by targeting a large number of protein-encoding genes and non-coding RNAs. In this study, we show that a microRNA, miR-200c, is a novel c-Myc target that promotes cellular transformation and metastasis in nasopharyngeal carcinoma. MiR-200c achieves this oncogenic effect, at least in part, by targeting and inhibiting the tumor suppressor gene PTEN (phosphatase and tensin homolog), which is a key inhibitor of the AKT kinase signaling that promotes tumorigenesis in nasopharyngeal carcinoma. Our study thus identifies cMyc-miR-200c-PTEN-AKT as a functional module that promotes cellular transformation in nasopharyngeal carcinoma.

Keywords: PTEN; c-Myc; miRNA-200c; nasopharyngeal carcinoma.

MeSH terms

  • Animals
  • Carcinoma / genetics
  • Carcinoma / pathology*
  • Cell Cycle
  • Cell Line, Tumor
  • Cell Movement
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mice
  • MicroRNAs / genetics*
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / genetics
  • Nasopharyngeal Neoplasms / pathology*
  • Neoplasm Metastasis
  • Neoplasm Transplantation
  • PTEN Phosphohydrolase / genetics*
  • Proto-Oncogene Proteins c-myc / genetics*
  • Transcriptional Activation*
  • Up-Regulation

Substances

  • MIRN200 microRNA, human
  • MYC protein, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-myc
  • PTEN Phosphohydrolase
  • PTEN protein, human