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RECK overexpression reduces invasive ability in ameloblastoma cells
Author(s) -
Liang Qixiang,
Liang Yancan,
Xu Zhiying,
Chen Weiliang,
Xie Hongliang,
Zhang Bin
Publication year - 2014
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12179
Subject(s) - transfection , ameloblastoma , angiogenesis , matrix metalloproteinase , metastasis , cancer research , microbiology and biotechnology , cell culture , biology , cell growth , hek 293 cells , downregulation and upregulation , gene , pathology , cancer , medicine , anatomy , genetics , maxilla
Background Ameloblastoma is a frequent odontogenic neoplasm characterized by local invasiveness and high risk of recurrence. Reversion‐inducing cysteine‐rich protein with K azal 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 h TERT + ‐ AM . Functional characteristics of h TERT + ‐ 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 m RNA and protein ( P < 0.01) was detected in RECK ‐transfected h TERT + ‐ AM cells. RECK overexpression caused a decrease in migration and invasion ( P < 0.01) for h TERT + ‐ 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 h TERT + ‐ AM cells, suggesting RECK may be a new target for ameloblastoma treatment.