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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/18350


    Title: The upregulation of metallothionein-1 expression in areca quid chewing-associated oral squamous cell carcinomas
    Authors: Lee, S.-S.;Yang, S.-F.;Ho, Y.-C.;Tsai, C.-H.;Chang, Y.-C.
    Keywords: Areca quid;Arecoline;Metallothionein-1;Oral squamous cell carcinoma;Regulatory mechanisms
    Date: 2008
    Issue Date: 2017-08-14T08:47:35Z (UTC)
    ISSN: 1368-8375
    Abstract: Metallothioneins (MTs) are a family of low molecular weight, cysteine-rich, inducible, intracellular proteins that bind heavy metals with high affinity. MT-1 is known as a stress-inducible protein and functions as an antioxidant enzyme. Areca quid chewing is a major risk factor in the development and further progression of oral squamous cell carcinoma (OSCC). The aim of this study was to compare MT-1 expression in normal human oral epithelium and OSCC and further explore the potential mechanism that may lead to induce MT-1 expression. Thirty four OSCC and 10 normal epithelium specimens were examined by immunohistochemistry and analyzed by the clinico-pathological profiles. The oral epithelial cell line GMN cells were challenged with arecoline, a major areca nut alkaloid, by reverse-transcriptase polymerase chain reaction. Furthermore, tobacco smoke carcinogen benzo[a]pyrene (BaP) and glutathione (GSH) precursor N-acetyl-l-cysteine (NAC) were added to find the possible regulatory mechanisms. The results from immunohistochemistry demonstrated that MT-1 expression was significantly higher in OSCC specimens (p < 0.05). No significant difference in MT-1 expression was observed with respect to age, sex, T category, and stage (p > 0.05). The high MT-1 expression was associated with lymph node metastasis (p = 0.012). In addition, arecoline was found to elevate MT-1 mRNA in a dose-dependent manner (p < 0.05). Furthermore, the addition of BaP enhanced the arecoline-induced MT-1expression (p < 0.05). The addition of NAC markedly inhibited the arecoline-induced MT-1expression (p < 0.05). These results lead to the conclusion that MT-1 expression is significantly upregulated in areca quid chewing associated-OSCC. The expression profile suggests MT-1 could be used clinically as a marker for tumors possessing the potential for lymph node metastasis. The compounds of tobacco products may act synergistically in the pathogenesis of OSCC in areca quid chewers. The regulation of MT-1 expression induced by arecoline is critically dependent on the intracellular GSH concentration. © 2007 Elsevier Ltd. All rights reserved.
    URI: http://dx.doi.org/10.1016/j.oraloncology.2007.01.019
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-38749087559&doi=10.1016%2fj.oraloncology.2007.01.019&partnerID=40&md5=528b7afa646bed76b72b4c4ba3ffff1a
    https://ir.csmu.edu.tw:8080/ir/handle/310902500/18350
    Relation: Oral Oncology 44 (2) ,180-186
    Appears in Collections:[牙醫學系暨碩士班] 期刊論文

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