Upregulation of heme oxygenase-1 expression in areca-quid-chewing-associated oral squamous cell carcinoma.

doi:10.1016/S0929-6646(08)60100-X

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题名:	Upregulation of heme oxygenase-1 expression in areca-quid-chewing-associated oral squamous cell carcinoma.
作者:	Lee, SS Yang, SF Tsai, CH Chou, MC Chou, MY Chang, YC
贡献者:	中山醫學大學
日期:	2008
上传时间:	2015-07-15T10:03:40Z (UTC)
ISSN:	0929-6646
摘要:	BACKGROUND/PURPOSE: Heme oxygenase-1 (HO-1) is known as an oxidative stress responsive protein that is upregulated by various physiologic and endogenous stimuli. HO-1 has been proposed to provide an important cellular response that protects cells against oxidative damage. Areca quid chewing is a major risk factor in the development and further progression of oral squamous cell carcinoma (OSCC). The aim of the present study was to investigate the difference in HO-1 expression in normal human oral epithelium and OSCC, and further explore the potential mechanism that may lead to HO-1 expression. METHODS: Thirty-five OSCC and 10 normal epithelium specimens were examined by immunohistochemistry and analyzed by clinicopathologic profiles. The oral epithelial GNM cell line was 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 were added to find the possible regulatory mechanisms. RESULTS: HO-1 expression was significantly higher in OSCC specimens (p < 0.05). No significant difference in HO-1 expression was observed with respect to age, sex, T category, and stage (p > 0.05). The high HO-1 expression was associated with lymph node metastasis (p = 0.005). In addition, arecoline was found to elevate HO-1 mRNA in a dose-dependent manner (p < 0.05). The addition of BaP enhanced arecolineinduced HO-1 expression (p < 0.05). Moreover, addition of NAC markedly inhibited arecoline-induced HO-1 expression (p < 0.05). CONCLUSION: Taken together, these results suggest that HO-1 expression is significantly upregulated in OSCC from areca quid chewers, and arecoline may be responsible for enhanced HO-1 expression in vivo. The compounds of cigarette smoke may act synergistically in the pathogenesis of areca-quid-chewing-associated OSCC. The regulation of HO-1 expression induced by arecoline is critically dependent on intracellular GSH concentration.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/11322 http://dx.doi.org/10.1016/S0929-6646(08)60100-X
關聯:	J Formos Med Assoc. 2008 May;107(5):355-63.
显示于类别:	[牙醫學系暨碩士班] 期刊論文

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