c-MYB regulates cell growth and DNA damage repair through modulating MiR-143

FEBS Lett. 2015 Feb 27;589(5):555-64. doi: 10.1016/j.febslet.2015.01.012. Epub 2015 Jan 20.

Abstract

Radiotherapy is the most successful nonsurgical treatment for nasopharyngeal carcinoma (NCP). Although NPCs initially respond well to a full course of radiation, recurrence and metastasis are frequent. In this study, we found that down-regulated c-MYB expression was associated with increased radiation resistance and DNA damage repair ability. Interestingly, c-MYB was over-expressed in cancer tissues but not in the adjacent tissues. Down-regulation of c-MYB expression inhibited cell proliferation, and led to cell cycle arrest at the M phase in NPC cells. Luciferase and chromatin immunoprecipitation assays demonstrated that c-MYB transactivated miR-143 through direct binding to its promoter. Based on these results, c-MYB might target miR-143 in order to regulate stem cell properties, cell growth, apoptosis, and DNA damage repair.

Keywords: Cancer stem cell; Nasopharyngeal carcinoma; Radio-resistivity; c-MYB; miR-143.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma
  • Cell Line
  • Cell Line, Tumor
  • DNA Damage / genetics*
  • Humans
  • In Vitro Techniques
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / genetics
  • Nasopharyngeal Neoplasms / metabolism
  • Neoplastic Stem Cells / metabolism
  • Neoplastic Stem Cells / radiation effects
  • Proto-Oncogene Proteins c-myb / genetics
  • Proto-Oncogene Proteins c-myb / metabolism*
  • Real-Time Polymerase Chain Reaction

Substances

  • MIRN143 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-myb