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首页> 外文期刊>Journal of Cellular Physiology >IL-1 beta Promotes Malignant Transformation and Tumor Aggressiveness in Oral Cancer
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IL-1 beta Promotes Malignant Transformation and Tumor Aggressiveness in Oral Cancer

机译：il - 1β促进恶性转化和在口腔癌肿瘤侵犯

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摘要

Chronic inflammation, coupled with alcohol, betel quid, and cigarette consumption, is associated with oral squamous cell carcinoma (OSCC). Interleukin-1 beta (IL-1 beta) is a critical mediator of chronic inflammation and implicated in many cancers. In this study, we showed that increased pro-IL-1 beta expression was associated with the severity of oral malignant transformation in a mouse OSCC model induced by 4-Nitroquinolin-1-oxide (4-NQO) and arecoline, two carcinogens related to tobacco and betel quid, respectively. Using microarray and quantitative PCR assay, we showed that pro-IL-1 beta was upregulated in human OSCC tumors associated with tobacco and betel quid consumption. In a human OSCC cell line TW2.6, we demonstrated nicotine-derived nitrosamine ketone (NNK) and arecoline stimulated IL-1 beta secretion in an inflammasome-dependent manner. IL-1 beta treatment significantly increased the proliferation and dysregulated the Akt signaling pathways of dysplastic oral keratinocytes (DOKs). Using cytokine antibodies and inflammation cytometric bead arrays, we found that DOK and OSCC cells secreted high levels of IL-6, IL-8, and growth-regulated oncogene-a following IL-1 beta stimulation. The conditioned medium of IL-1 beta-treated OSCC cells exerted significant proangiogenic effects. Crucially, IL-1 beta increased the invasiveness of OSCC cells through the epithelial-mesenchymal transition (EMT), characterized by downregulation of E-cadherin, upregulation of Snail, Slug, and Vimentin, and alterations in morphology. These findings provide novel insights into the mechanism underlying OSCC tumorigenesis. Our study suggested that IL-1 beta can be induced by tobacco and betel quid-related carcinogens, and participates in the early and late stages of oral carcinogenesis by increasing the proliferation of dysplasia oral cells, stimulating oncogenic cytokines, and promoting aggressiveness of OSCC. (C) 2014 Wiley Periodicals, Inc.
机译：慢性炎症,再加上酒精,槟榔英镑,香烟消费,是相关的与口腔鳞状细胞癌(OSCC)。Interleukin-1ββ(il - 1)是至关重要的慢性炎症和涉及的中介在许多癌症。增加pro-IL-1β表达有关口腔恶性的严重程度转换在鼠标OSCC模型引起的4-Nitroquinolin-1-oxide (4-NQO)和槟榔碱,两种致癌物有关烟草和槟榔分别为英镑。定量PCR分析,我们发现pro-IL-1β是调节人类OSCC肿瘤与烟草和槟榔有关消费。证明nicotine-derived亚硝胺酮(NNK)和槟榔碱刺激il - 1β分泌inflammasome-dependent方式。il - 1β治疗显著增加核扩散和特异表达一种蛋白激酶信号通道的发育不良的口腔角质细胞(辩)。使用细胞因子抗体和炎症仪珠数组,我们发现辩经OSCC细胞分泌il - 6水平高,引发,和growth-regulated oncogene-a il - 1β刺激。beta-treated OSCC细胞施加显著proangiogenic效果。增加OSCC细胞的侵袭性epithelial-mesenchymal过渡(EMT),的差别表现为对这些钙upregulation的蜗牛、蛞蝓和波形蛋白,改变形态。小说OSCC机制的见解肿瘤发生。可以诱导烟草和槟榔quid-related吗致癌物质,参与早期的和晚期口腔致癌作用的增加发育不良的口腔细胞的增殖,刺激致癌细胞因子,促进OSCC的攻击性。期刊、公司。

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