Liang Qi-xiang, Liang Yan-can, Xu Zhi-ying, Chen Wei-liang, Xie Hong-liang, Zhang Bin
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.
J Oral Pathol Med. 2014 Sep;43(8):613-8. doi: 10.1111/jop.12179. Epub 2014 Mar 20.
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.
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.
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).
Overexpression of RECK gene significantly inhibited cell invasive ability of hTERT(+) -AM cells, suggesting RECK may be a new target for ameloblastoma treatment.
成釉细胞瘤是一种常见的牙源性肿瘤，具有局部侵袭性和高复发风险。富含Kazal基序的逆转录诱导富含半胱氨酸蛋白（RECK）是一种抑制转移和血管生成的肿瘤抑制因子。本研究旨在探讨RECK过表达对成釉细胞瘤细胞侵袭潜能的影响。
构建含人RECK基因的慢病毒载体，随后将其稳定转染至永生化成釉细胞瘤细胞系hTERT(+) -AM中。通过酶谱法或市售检测方法，对稳定过表达RECK的hTERT(+) -AM细胞的增殖、迁移、侵袭以及基质金属蛋白酶（MMP）-2、MMP-9的调节等功能特性进行检测。
在转染RECK的hTERT(+) -AM细胞中检测到RECK mRNA和蛋白的稳定且高表达（P < 0.01）。RECK过表达导致hTERT(+) -AM细胞的迁移和侵袭能力降低（P < 0.01），同时MMP-2、MMP-9的活性降低（P < 0.01）。增殖不受RECK过表达的影响（P > 0.05）。
RECK基因过表达显著抑制hTERT(+) -AM细胞的侵袭能力，提示RECK可能成为成釉细胞瘤治疗的新靶点。
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