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Staphylococcus aureus induces COX-2-dependent proliferation and malignant transformation in oral keratinocytes.
Journal of Oral Microbiology ( IF 4.5 ) Pub Date : 2019-07-22 , DOI: 10.1080/20002297.2019.1643205
Yuxia Wang 1, 2, 3 , Shiyu Liu 1, 2 , Bolei Li 1, 2 , Yaling Jiang 1, 2 , Xinxuan Zhou 1 , Jing Chen 1, 2 , Mingyun Li 1 , Biao Ren 1 , Xian Peng 1 , Xuedong Zhou 1, 2 , Lei Cheng 1, 2
Affiliation  

The COX-2/PGE2 axis can play roles in mediating the progression of tumor. COX-2 induction was observed in oral cancer. In our previous study, we found Staphylococcus aureus, a pathogen prevalent in oral cancer, can activate the COX-2/PGE2 pathway in human oral keratinocyte (HOK) cells. Here, we investigated the proliferation of HOK cells affected by COX-2 induction and the role of COX-2 induction in the malignant transformation of HOK cells. We found S. aureus was able to facilitate HOK cell proliferation through upregulating COX-2 expression. With the induction of COX-2, expression of oral cancer-associated genes cyclin D1 was upregulated and p16 was downregulated. Transcriptome analysis showed that the “NF−kappa B signaling pathway” and “TNF signaling pathway” had the highest enrichment of differentially expressed genes (DEGs) with COX-2 over-expression. Seven upregulated genes (juntlr4cxcl1lifcxcl3, tnfrsf1β, and il1β) in these two pathways were critical for the increased proliferation of HOK cells and might be associated with COX-2. Malignant transformation of cells was evaluated by soft agar colony formation assay and S. aureus infection promoted HOK cell colony formation. These results suggest the potential of S. aureus to induce the infection-associated malignant transformation of oral epitheliums through COX-2 activation.



中文翻译:

金黄色葡萄球菌在口腔角质形成细胞中诱导COX-2依赖性增殖和恶性转化。

COX-2 / PGE 2 轴可在介导肿瘤进展中发挥作用。在口腔癌中观察到COX-2诱导。在我们先前的研究中,我们发现 金黄色葡萄球菌(一种在口腔癌中普遍存在的病原体)可以激活 人口腔角质形成细胞(HOK)细胞中的COX-2 / PGE 2途径。在这里,我们调查了受OKX-2诱导影响的HOK细胞的增殖以及COX-2诱导在HOK细胞恶性转化中的作用。我们发现 金黄色葡萄球菌 能够通过上调COX-2表达来促进HOK细胞增殖。随着COX-2的诱导,口腔癌相关基因 cyclin D1的 表达上调,  p16 被下调了。转录组分析显示,“NF-κB信号传导途径”和“ TNF信号传导途径”具有COX-2过表达的差异表达基因(DEG)富集程度最高。这两个途径中的七个上调基因(jun,  tlr4,  cxcl1,  lif,  cxcl3 tnfrsf1β和 il1β)对于HOK细胞增殖的增加至关重要,并且可能与COX-2相关。通过软琼脂菌落形成试验评价细胞的恶性转化, 金黄色葡萄球菌 感染促进了HOK细胞菌落的形成。这些结果表明金黄色葡萄球菌的潜力  通过COX-2激活诱导口腔上皮的感染相关恶性转化。

更新日期:2019-07-22
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