Department of Oral and Maxillofacial Surgery, Second Affiliated Hospital, Sun Yat-Sen University, 107 Yanjiang Road West, Guangzhou, Guangdong, 510120, PR China.
BMC Cancer. 2009 Dec 8;9:427. doi: 10.1186/1471-2407-9-427.
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 aim of this study was to characterize the relationship between RECK and MMP-2 expression and the clinical manifestation of ameloblastoma.
Immunohistochemistry 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.
RECK 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).
Low 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.
成釉细胞瘤是一种常见的牙源性良性肿瘤，其特征为局部侵袭性、高复发风险和偶发转移及恶性转化。基质金属蛋白酶-2（MMP-2）通过破坏细胞外基质（ECM）和基底膜促进肿瘤的侵袭和进展。为了实现这种蛋白水解活性，内源性抑制剂是富含半胱氨酸的逆转录诱导 Kazal 基序蛋白（RECK）。本研究旨在探讨 RECK 与 MMP-2 的表达与成釉细胞瘤临床表现之间的关系。
采用免疫组织化学和逆转录聚合酶链反应（RT-PCR）检测角化囊性牙源性肿瘤（KCOT）、成釉细胞瘤和造釉细胞瘤中的 RECK 和 MMP-2 蛋白和 mRNA 表达。
RECK 蛋白表达在 KCOT（87.5%）、成釉细胞瘤（56.5%）和造釉细胞瘤（0%）中显著降低（P < 0.01），且在复发性成釉细胞瘤中明显低于原发性成釉细胞瘤（P < 0.01），但与成釉细胞瘤的组织学类型无关。MMP-2 蛋白表达在成釉细胞瘤和造釉细胞瘤中明显高于 KCOT（P < 0.01）。RECK mRNA 表达在成釉细胞瘤中明显低于 KCOT（P < 0.01），在复发性成釉细胞瘤中低于原发性成釉细胞瘤，在造釉细胞瘤中为阴性。MMP-2 mRNA 表达在成釉细胞瘤中明显高于 KCOT（P < 0.01），但在复发性成釉细胞瘤与原发性成釉细胞瘤之间无差异。RECK 蛋白表达与成釉细胞瘤中 MMP-2 蛋白表达呈负相关（r = -0.431，P < 0.01）。
RECK 低表达或无表达及 MMP-2 表达增加可能与成釉细胞瘤的不良临床结果相关。RECK 可能通过调节 MMP-2 的转录后水平参与成釉细胞瘤的侵袭、复发和恶性转化。
