miR-206 enhances nasopharyngeal carcinoma radiosensitivity by targeting IGF1

Kaohsiung J Med Sci. 2017 Sep;33(9):427-432. doi: 10.1016/j.kjms.2017.05.015. Epub 2017 Jul 10.

Abstract

Radioresistance remains a major problem in nasopharyngeal carcinoma (NPC) treatment. However, the underlying molecular mechanisms of NPC radioresistance remain poorly understood. The present study aimed to investigate the potential role and mechanism of miR-206 in NPC radioresistance. We observed that miR-206 was down-regulated in radioresistant NPC cells. Furthermore, restoration of miR-206 in CNE2-IR cells suppressed enhanced radiosensitivity of NPC cells. In contrast, inhibition of miR-206 in CNE2 cells reduced the radiosensitivity. We also found that miR-206 directly targeted IGF1 and inhibited the PI3K/AKT pathway. Our data demonstrate that miR-206 sensitizes NPC cell to irradiation by targeting IGF1, highlighting the therapeutic potential of miR-206 in NPC radiosensitization.

Keywords: IGF1; Nasopharyngeal carcinoma; PI3K/AKT pathway; Radioresistance; miR-206.

MeSH terms

  • Antagomirs / genetics
  • Antagomirs / metabolism
  • Base Sequence
  • Binding Sites
  • Cell Line, Tumor
  • Gamma Rays
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Insulin-Like Growth Factor I / genetics*
  • Insulin-Like Growth Factor I / metabolism
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Nasopharynx / metabolism
  • Nasopharynx / pathology
  • Nasopharynx / radiation effects*
  • Phosphatidylinositol 3-Kinases / genetics
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Radiation Tolerance / genetics*
  • Signal Transduction

Substances

  • Antagomirs
  • MicroRNAs
  • Mirn206 microRNA, mouse
  • insulin-like growth factor-1, mouse
  • Insulin-Like Growth Factor I
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt