ArticleBMC cancer2009
Expression of RECK and matrix metalloproteinase-2 in ameloblastoma.
Article in BMC cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 36 citations in OpenAlex.
- Title of the article: diagnostic markers for odontogenic tumors: an insight: a review.Discover oncology · 2024Review
- Factors Associated with Recurrence of Ameloblastoma: A Scoping Review.Head and neck pathology · 2024Article
- Bioengineering the ameloblastoma tumour to study its effect on bone nodule formation.Scientific reports · 2021Article
- Article
- The Many Facets of Metzincins and Their Endogenous Inhibitors: Perspectives on Ovarian Cancer Progression.International journal of molecular sciences · 2018Review
- Potential Role of Reversion-Inducing Cysteine-Rich Protein with Kazal Motifs (RECK) in Regulation of Matrix Metalloproteinases (MMPs) Expression in Periodontal Diseases.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Bioinformatics Analysis Reveals Genes Involved in the Pathogenesis of Ameloblastoma and Keratocystic Odontogenic Tumor.International journal of molecular and cellular medicine · 2016Article
- RECK controls breast cancer metastasis by modulating a convergent, STAT3-dependent neoangiogenic switch.Oncogene · 2015Article
- Immunohistochemical expression of Type IV Collagen and Autocrine Motility Factor Receptor in Odontogenic Tumours.Journal of clinical and diagnostic research : JCDR · 2014Article
- Size matters: sequential mutations in tumorigenesis may reflect the stochastic effect of mutagen target sizes.Genes & cancer · 2011Article
- Molecular markers of tumor invasiveness in ameloblastoma: An update.Annals of maxillofacial surgery · 2011Article
- Literature review of 86 cases of mandibular ameloblastic carcinoma.National journal of maxillofacial surgeryReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmeloblastoma is a frequent odontogenic benign tumor characterized by local invasiveness, high risk of recurrence and occasional metastasis and malignant transformation. Matrix metalloproteinase-2 (MMP-2) promotes tumor invasion and progression by destroying the extracellular matrix (ECM) and basement membrane. For this proteolytic activity, the endogenous inhibitor is reversion-inducing cysteine rich protein with Kazal motifs (RECK). The aim of this study was to characterize the relationship between RECK and MMP-2 expression and the clinical manifestation of ameloblastoma.
methodsImmunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) were employed to detect the protein and mRNA expression of RECK and MMP-2 in keratocystic odontogenic tumor (KCOT), ameloblastoma and ameloblastic carcinoma.
resultsRECK protein expression was significantly reduced in KCOT (87.5%), ameloblastoma (56.5%) and ameloblastic carcinoma (0%) (P < 0.01), and was significantly lower in recurrent ameloblastoma compared with primary ameloblastoma (P < 0.01), but did not differ by histological type of ameloblastoma. MMP-2 protein expression was significantly higher in ameloblastoma and ameloblastic carcinoma compared with KCOT (P < 0.01). RECK mRNA expression was significantly lower in ameloblastoma than in KCOT (P < 0.01), lower in recurrent ameloblastoma than in primary ameloblastoma, and was negative in ameloblastic carcinoma. MMP-2 mRNA expression was significantly higher in ameloblastoma compared with KCOT (P < 0.01), but was no different in recurrent ameloblastoma versus primary ameloblastoma. RECK protein expression was negatively associated with MMP-2 protein expression in ameloblastoma (r = -0.431, P < 0.01).
conclusionLow or no RECK expression and increased MMP-2 expression may be associated with negative clinical findings in ameloblastoma. RECK may participate in the invasion, recurrence and malignant transformation of ameloblastoma by regulating MMP-2 at the post-transcriptional level.
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