title: RECK overexpression reduces invasive ability in ameloblastoma cells.
abstract: BACKGROUND
  Ameloblastoma is a frequent odontogenic neoplasm characterized by local invasiveness and high risk of recurrence. Reversion-inducing cysteine-rich protein with Kazal motifs (RECK) is a tumor suppressor that inhibits metastasis and angiogenesis. The aim of this study was to investigate effects of RECK overexpression on invasive potential in ameloblastoma cells.
  
  
  METHODS
  Lentiviral vectors containing human RECK gene were created and subsequently stably transfected into immortalized ameloblastoma cell line hTERT(+) -AM. Functional characteristics of hTERT(+) -AM cells with stable RECK overexpression included proliferation, migration, invasion, and regulation of matrix metalloproteinases (MMP)-2, MMP-9 measured by zymography or commercially available assays.
  
  
  RESULTS
  The stable and higher expression of RECK mRNA and protein (P < 0.01) was detected in RECK-transfected hTERT(+) -AM cells. RECK overexpression caused a decrease in migration and invasion (P < 0.01) for hTERT(+) -AM cells and a decrease in activity of MMP-2, MMP-9 (P < 0.01). Proliferation was not affected by RECK overexpression (P > 0.05).
  
  
  CONCLUSIONS
  Overexpression of RECK gene significantly inhibited cell invasive ability of hTERT(+) -AM cells, suggesting RECK may be a new target for ameloblastoma treatment.
authors.affiliation: Department of Oral and Maxillofacial Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China; Key Laboratory of Malignant Tumor Gene Regulation and Target Therapy of Guangzhou Higher Education Institutes, Sun Yat-sen University, Guangzhou, Guangdong, China.
authors.forename: Qi-xiang
authors.initials: QX
authors.lastname: Liang
authors.forename: Yan-can
authors.initials: YC
authors.lastname: Liang
authors.forename: Zhi-ying
authors.initials: ZY
authors.lastname: Xu
authors.forename: Wei-liang
authors.initials: WL
authors.lastname: Chen
authors.forename: Hong-liang
authors.initials: HL
authors.lastname: Xie
authors.forename: Bin
authors.initials: B
authors.lastname: Zhang
mesh_terms: D000564:Ameloblastoma / Q000737:chemistry* / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000502:physiology; D049109:Cell Proliferation; D002470:Cell Survival / Q000502:physiology; D058851:GPI-Linked Proteins / Q000032:analysis*; D015971:Gene Expression Regulation, Enzymologic / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D005822:Genetic Vectors / Q000235:genetics; D006801:Humans; D016086:Lentivirus / Q000235:genetics; D020778:Matrix Metalloproteinase 2 / Q000032:analysis; D020780:Matrix Metalloproteinase 9 / Q000032:analysis; D009361:Neoplasm Invasiveness; D014162:Transfection
chemical_list: D058851:GPI-Linked Proteins; C115460:RECK protein, human; C522361:MMP2 protein, human; D020778:Matrix Metalloproteinase 2; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9
keywords: ameloblastoma; invasion; matrix metalloproteinase; reversion-inducing cysteine-rich protein with Kazal motifs