Knockdown of miR-214 promotes apoptosis and inhibits cell proliferation in nasopharyngeal carcinoma

PLoS One. 2014 Jan 21;9(1):e86149. doi: 10.1371/journal.pone.0086149. eCollection 2014.

Abstract

MicroRNA-214 (MiR-214) is aberrantly expressed in several human tumors such as ovarian cancer and breast cancer. However, the role of miR-214 in nasopharyngeal carcinoma (NPC) is still unknown. In this study, we report that miR-214 was overexpressed in NPC cell lines and tissues. Silencing of miR-214 by LNA-antimiR-214 in NPC cells resulted in promoting apoptosis and suppressing cell proliferation in vitro, and suppressed tumor growth in nude mice in vivo. Luciferase reporter assay was performed to identify Bim as a direct target of miR-214. Furthermore, this study showed that low Bim expression in NPC tissues correlated with poor survival of NPC patients. Taken together, our findings suggest that miR-214 plays an important role in NPC carcinogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Animals
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis* / genetics
  • Base Sequence
  • Bcl-2-Like Protein 11
  • Carcinogenesis / genetics
  • Carcinogenesis / pathology
  • Carcinoma
  • Cell Line, Tumor
  • Cell Proliferation
  • Female
  • Follow-Up Studies
  • Gene Expression Regulation, Neoplastic
  • Gene Knockdown Techniques*
  • Gene Silencing
  • Humans
  • Male
  • Membrane Proteins / genetics
  • Mice
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Middle Aged
  • Molecular Sequence Data
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / genetics*
  • Nasopharyngeal Neoplasms / pathology*
  • Proto-Oncogene Proteins / genetics
  • Survival Analysis
  • Treatment Outcome
  • Young Adult

Substances

  • Apoptosis Regulatory Proteins
  • BCL2L11 protein, human
  • Bcl-2-Like Protein 11
  • Bcl2l11 protein, mouse
  • MIRN214 microRNA, human
  • Membrane Proteins
  • MicroRNAs
  • Proto-Oncogene Proteins

Grant support

This work was supported grants from the National High Technology Research and Development Program of China (863 Program) (No. 2012AA02A501); the Chinese State Key Basic Research Project (No. 2011CB504805); The National Natural Science Fund (No. 81272952); and a State Key Laboratory Grant to the Sun Yat-sen University Cancer Center. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.