miR-221 and miR-222 expression increased the growth and tumorigenesis of oral carcinoma cells

J Oral Pathol Med. 2011 Aug;40(7):560-6. doi: 10.1111/j.1600-0714.2010.01005.x. Epub 2011 Jan 13.

Abstract

Backgrounds: MicroRNAs are small noncoding RNAs involved in posttranscriptional gene regulation, which play an important role in both physiological functioning and pathological progression. The miR-221/miR-222 microRNA family has been shown to be related to the neoplastic process in a number of different types of cancers; nevertheless, its function in oral squamous cell carcinoma (OSCC) remained uncertain.

Materials and methods: Paired OSCC and matched noncancerous oral mucosa were examined for miR-221/miR-222 expression using quantitative reverse-transcription PCR. Ectopic expression of miR-221/miR-222 by lentiviral infection was investigated to explore its in vitro and in vivo impact on the oncogenic phenotype and the expression of various target genes. The expression of Cip/Kip cell cycle regulator p27 in tumors was analyzed with immunohistochemistry.

Results: The expression levels of miR-221 and miR-222 were highly correlated in OSCC. Increased miR-221/miR-222 expression was found in 40% of OSCC tissues. The ectopic expression of miR-221 or of miR-222 increased growth and anchorage-independent colony formation of OSCC cell lines. It also resulted in an increase in the tumorigenesis of an OSCC cell line in nude mice. Western blot analysis suggested that p27 and p57 might be the targets of miR-221/miR-222. p27 expression was reversely associated with the miR-221 and miR-222 expression level in OSCC tissues.

Conclusions: Our findings suggested that increased miR-221/miR-222 expression was associated with the OSCC cell growth.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alphapapillomavirus / isolation & purification
  • Animals
  • Carcinoma, Squamous Cell / pathology*
  • Carcinoma, Squamous Cell / virology
  • Case-Control Studies
  • Cell Line, Tumor
  • Cell Movement / physiology
  • Cell Proliferation
  • Cyclin-Dependent Kinase Inhibitor p27 / analysis
  • Cyclin-Dependent Kinase Inhibitor p57 / analysis
  • Disease Progression
  • Genetic Vectors / genetics
  • Humans
  • Lentivirus / genetics
  • Male
  • Mice
  • Mice, Nude
  • MicroRNAs / analysis*
  • Middle Aged
  • Mouth Mucosa / pathology
  • Mouth Neoplasms / pathology*
  • Mouth Neoplasms / virology
  • Neoplasm Transplantation
  • Phenotype
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • CDKN1B protein, human
  • CDKN1C protein, human
  • Cyclin-Dependent Kinase Inhibitor p57
  • MIRN221 microRNA, human
  • MIRN222 microRNA, human
  • MicroRNAs
  • Cyclin-Dependent Kinase Inhibitor p27