Fusobacterium nucleatum Caused DNA Damage and Promoted Cell Proliferation by the Ku70/p53 Pathway in Oral Cancer Cells
Fusobacterium nucleatum Caused DNA Damage and Promoted Cell Proliferation by the Ku70/p53 Pathway in Oral Cancer Cells
复制标题
具核梭杆菌通过 Ku70/p53 通路引起口腔癌细胞 DNA 损伤并促进细胞增殖
DOI：
10.1089/dna.2019.5064
复制
发表时间：
2019-11-25
影响因子：
3.1
通讯作者：
Pan, Yaping
中科院分区：
文献类型：
--
作者：
Geng, Fengxue;Zhang, Yunjia;Pan, Yaping
细菌感染通过引起DNA损伤影响基因组的稳定性和完整性，从而增加肿瘤发生和发展的可能性。本研究旨在探讨牙周致病菌具核梭杆菌是否通过引起DNA双链断裂（DSB）而促进口腔鳞状细胞癌（OSCC）的发生。用F.核质。免疫印迹法和免疫荧光法检测γ H2 AX的表达。CCK-8法检测细胞增殖活性，流式细胞仪检测细胞周期变化。Ku 70、p53和p27的表达水平通过实时定量聚合酶链反应和蛋白质印迹法进行评估。质粒用于Ku 70的过表达以验证Ku 70和p53之间的可能关系。我们证实了在对F的反应中存在DSB。通过检测γ H2 AX的表达来检测核质。随着细胞周期的加快，细胞增殖能力增强，p27表达降低。Ku 70和野生型p53表达下调。当Ku 70过表达时，野生型p53对F.核质感染被上调，细胞增殖相应地被抑制。我们的结论是F. nucleatum感染通过Ku 70/p53途径引起DNA损伤，促进Tca 8113细胞增殖。
Bacterial infection influences genomic stability and integrity by causing DNA damage, which increases the possibility of tumor initiation and development. We aimed to investigate whether Fusobacterium nucleatum, one of the periodontal pathogens, promoted oral squamous cell carcinoma (OSCC) by causing DNA double-strand break (DSB). Tca8113 tongue squamous cell carcinoma cells were infected with F. nucleatum. The expression of gamma H2AX was detected by western blots and immunofluorescence. The proliferation and cell cycle alterations were tested by CCK8 and flow cytometry, respectively. The expression levels of Ku70, p53, and p27 were evaluated by quantitative real-time polymerase chain reaction and western blots. A plasmid was used for the overexpression of Ku70 to verify the possible relationship between Ku70 and p53. We confirmed the presence of DSBs in the response to F. nucleatum by detecting the expression of gamma H2AX. The cell proliferation ability was increased with an accelerated cell cycle while the expression of p27 was decreased. Meanwhile, the expression of Ku70 and wild p53 was downregulated. When Ku70 was overexpressed, the expression of wild p53 in response to F. nucleatum infection was upregulated and cell proliferation was accordingly inhibited. We concluded that F. nucleatum infection promoted the proliferation ability of Tca8113 by causing DNA damage via the Ku70/p53 pathway.