miR-16 induction after CDK4 knockdown is mediated by c-Myc suppression and inhibits cell growth as well as sensitizes nasopharyngeal carcinoma cells to chemotherapy

Tumour Biol. 2016 Feb;37(2):2425-33. doi: 10.1007/s13277-015-3966-1. Epub 2015 Sep 17.

Abstract

Cyclin-dependent kinase 4 (CDK4) is a member of cyclin-dependent kinase family which regulates G1 to S cell cycle transition. CDK4 activity is increased in many tumor types. Here, we report a negative automodulatory feedback loop between CDK4 and miR-16 that regulates cell cycle progression in nasopharyngeal carcinoma (NPC). By miRNA array and real-time PCR, we identified upregulation of tumor suppressor miR-16a, which inhibited cell cycle progression and sensitized NPC cells to chemotherapy. CDK4 knockdown reduced the expression of c-Myc, the latter of which directly suppresses the miR-16 expression by directly binding to the miR-16 promoter. Moreover, we found that miR-16 upregulation could reduce CDK4 expression by repressing CCND1 and thus forms a feedback loop via the CDK4/c-Myc/miR-16/CCND1 pathway. Finally, miR-16 was negatively correlated with CDK4 expression in NPC biopsies. In summary, our results define a double-negative feedback loop involving CDK4 and miR-16 mediated by c-Myc that modulates NPC cell growth and chemotherapy sensitivity.

Keywords: CDK4; Feedback loop; NPC; c-Myc; miR-16.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Carcinoma
  • Cell Cycle / drug effects
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cell Proliferation / genetics*
  • Cyclin D1 / genetics
  • Cyclin-Dependent Kinase 4 / genetics*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Gene Expression Regulation, Neoplastic / genetics
  • Gene Knockdown Techniques / methods
  • Genes, Tumor Suppressor / drug effects
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • MicroRNAs / genetics*
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / drug therapy
  • Nasopharyngeal Neoplasms / genetics*
  • Proto-Oncogene Proteins c-myc / genetics*
  • Up-Regulation / drug effects
  • Up-Regulation / genetics

Substances

  • Antineoplastic Agents
  • MIRN16 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-myc
  • Cyclin D1
  • CDK4 protein, human
  • Cyclin-Dependent Kinase 4