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首页> 外文期刊>Oral diseases >Hypoxia inducible factor-1alpha expression in areca quid chewing-associated oral squamous cell carcinomas.
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Hypoxia inducible factor-1alpha expression in areca quid chewing-associated oral squamous cell carcinomas.

机译：缺氧诱导因子-1α在槟榔咀嚼相关的口腔鳞状细胞癌中的表达。

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OBJECTIVES: Hypoxia inducible factor (HIF)-1alpha gene expression is mainly induced by tissue hypoxia. Overexpression of HIF-1alpha has been demonstrated in a variety of cancers. The aim of this study was to compare HIF-1alpha expression in normal human oral epithelium and areca quid chewing-associated oral squamous cell carcinoma (OSCC) and further to explore the potential mechanisms that may lead to induce HIF-1alpha expression. METHODS: Twenty-five OSCC from areca quid chewing-associated OSCC and 10 normal oral tissue biopsy samples without areca quid chewing were analyzed by immunohistochemistry. The oral epithelial cell line GNM cells were challenged with arecoline, a major areca nut alkaloid, by using Western blot analysis. Furthermore, glutathione precursor N-acetyl-l-cysteine (NAC), AP-1 inhibitor curcumin, extracellular signal-regulated protein kinase inhibitor PD98059, and protein kinase C inhibitor staurosporine were added to find the possible regulatory mechanisms. RESULTS: Hypoxia inducible factor-1alpha expression was significantly higher in OSCC specimens than normal specimen (P<0.05). Arecoline was found to elevate HIF-1alpha expression in a dose- and time-dependent manner (P<0.05). The addition of NAC, curcumin, PD98059, and staurosporine markedly inhibited the arecoline-induced HIF-1alpha expression (P<0.05). CONCLUSIONS: Hypoxia inducible factor-1alpha expression is significantly upregulated in areca quid chewing-associated OSCC and HIF-1alpha expression induced by arecoline is downregulated by NAC, curcumin, PD98059, and staurosporine.
机译：目的：缺氧诱导因子（HIF）-1alpha基因表达主要是由组织缺氧诱导的。 HIF-1alpha的过表达已在多种癌症中得到证实。这项研究的目的是比较正常人口腔上皮细胞和槟榔咀嚼相关的口腔鳞状细胞癌（OSCC）中的HIF-1alpha表达，并进一步探讨可能诱导HIF-1alpha表达的潜在机制。方法：采用免疫组织化学方法对25例槟榔咀嚼相关的OSCC和10例无槟榔咀嚼的正常口腔组织活检样本进行了分析。通过使用蛋白质印迹分析，用槟榔碱（一种主要的槟榔生物碱）攻击口腔上皮细胞系GNM细胞。此外，添加了谷胱甘肽前体N-乙酰基-1-半胱氨酸（NAC），AP-1抑制剂姜黄素，细胞外信号调节的蛋白激酶抑制剂PD98059和蛋白激酶C抑制剂星形孢菌素，以寻找可能的调节机制。结果：OSCC标本中缺氧诱导因子-1α的表达明显高于正常标本（P <0.05）。发现槟榔碱以剂量和时间依赖性方式升高HIF-1α表达（P <0.05）。 NAC，姜黄素，PD98059和星形孢菌素的添加显着抑制槟榔碱诱导的HIF-1alpha表达（P <0.05）。结论：NAC，姜黄素，PD98059和星形孢菌素可降低缺氧诱导因子-1α在槟榔咀嚼相关OSCC中的表达，而槟榔碱诱导的HIF-1alpha表达则下调。

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