title: miR-221 and miR-222 expression increased the growth and tumorigenesis of oral carcinoma cells.
abstract: BACKGROUND
  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.
  
  
  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.
authors.affiliation: Institute of Oral Biology, School of Dentistry, National Yang-Ming University, Taipei, Taiwan Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan.
authors.forename: Chun-Ju
authors.initials: CJ
authors.lastname: Yang
authors.forename: Wilma Grace
authors.initials: WG
authors.lastname: Shen
authors.forename: Chung-Ji
authors.initials: CJ
authors.lastname: Liu
authors.forename: Yun-Wen
authors.initials: YW
authors.lastname: Chen
authors.forename: Hsuan-Hsuan
authors.initials: HH
authors.lastname: Lu
authors.forename: Meng-Miao
authors.initials: MM
authors.lastname: Tsai
authors.forename: Shu-Chun
authors.initials: SC
authors.lastname: Lin
mesh_terms: D052685:Alphapapillomavirus / Q000302:isolation & purification; D000818:Animals; D002294:Carcinoma, Squamous Cell / Q000473:pathology* / Q000821:virology; D016022:Case-Control Studies; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000502:physiology; D049109:Cell Proliferation; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000032:analysis; D050761:Cyclin-Dependent Kinase Inhibitor p57 / Q000032:analysis; D018450:Disease Progression; D005822:Genetic Vectors / Q000235:genetics; D006801:Humans; D016086:Lentivirus / Q000235:genetics; D008297:Male; D051379:Mice; D008819:Mice, Nude; D035683:MicroRNAs / Q000032:analysis*; D008875:Middle Aged; D009061:Mouth Mucosa / Q000473:pathology; D009062:Mouth Neoplasms / Q000473:pathology* / Q000821:virology; D009368:Neoplasm Transplantation; D010641:Phenotype; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D050760:Cyclin-Dependent Kinase Inhibitor p27; D050761:Cyclin-Dependent Kinase Inhibitor p57; D035683:MicroRNAs; C436291:CDKN1B protein, human; C493964:CDKN1C protein, human; C525709:MIR221, human; C525710:MIR222, human