MiR-214 reduces cell survival and enhances cisplatin-induced cytotoxicity via down-regulation of Bcl2l2 in cervical cancer cells

FEBS Lett. 2013 Mar 1;587(5):488-95. doi: 10.1016/j.febslet.2013.01.016. Epub 2013 Jan 18.

Abstract

MiR-214 has been shown to inhibit cell growth, migration and invasion. Here we demonstrate that ectopic expression of miR-214 reduces cell survival, induces apoptosis and enhances sensitivity to cisplatin through directly inhibiting Bcl2l2 expression in cervical cancer HeLa and C-33A cells. Further analysis reveals that apoptosis induced by miR-214 is correlated with increased expression of Bax, caspase-9, caspase-8 and caspase-3. Moreover, we show that miR-214 is regulated by DNA methylation and histone deacetylation. Taken together, these data suggest that miR-214 might be a candidate target for the development of novel therapeutic strategies to treat cervical cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation
  • Antineoplastic Agents / pharmacology*
  • Apoptosis
  • Apoptosis Regulatory Proteins / genetics*
  • Apoptosis Regulatory Proteins / metabolism
  • Base Sequence
  • Binding Sites
  • Caspases / genetics
  • Caspases / metabolism
  • Cell Survival*
  • Cisplatin / pharmacology*
  • DNA Methylation
  • Down-Regulation
  • Drug Resistance, Neoplasm
  • Enzyme Activation
  • Gene Expression
  • Gene Expression Regulation, Neoplastic
  • HeLa Cells
  • Histones / metabolism
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • MicroRNAs / physiology*
  • Protein Processing, Post-Translational
  • RNA Interference

Substances

  • Antineoplastic Agents
  • Apoptosis Regulatory Proteins
  • BCL2L2 protein, human
  • Histones
  • MIRN214 microRNA, human
  • MicroRNAs
  • Caspases
  • Cisplatin