Expression of RECK and matrix metalloproteinase-2 in ameloblastoma

Bin Zhang,Hong-Liang Xie,Jin Zhang,Zhi-Ying Xu

doi:10.1186/1471-2407-9-427

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.

Highlights

Ameloblastoma is a frequent odontogenic benign tumor characterized by local invasiveness, high risk of recurrence and occasional metastasis and malignant transformation
Expression of RECK and Matrix metalloproteinase-2 (MMP-2) protein in KOCT, ameloblastoma and ameloblastic carcinoma Immunoreactivity for RECK was detected in most epithelial cells of KOCT, in central polyhedral cells of follicular ameloblastoma and in peripheral columnar cells of plexiform ameloblastoma, but not in ameloblastic carcinoma cells (Figure 1)
RECK expression gradually significantly decreased in keratocystic odontogenic tumor (KCOT) (87.5%), ameloblastoma (56.52%) and ameloblastic carcinoma (0%, P < 0.01), and was significantly higher in primary ameloblastoma (71.11%) than in recurrent ameloblastoma (29.17%, P < 0.01), but no significant difference was seen between histological types (Table 1)

Summary

Introduction

Ameloblastoma 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 key action of RECK is to inhibit MMPs, especially MMP-2 and MMP-9 [6] For this reason, it is important in embryogenesis and other physiological processes. RECK expression in pancreatic cancer tissue was significantly lower than in adjacent normal tissues and was negatively associated with MMP-2 activation and tumor invasive ability [7]. This study investigated the combinatorial role and association of RECK and MMP-2 in ameloblastoma

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