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Updated: Jun 27, 2025

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The Soft Agar Colony Formation Assay
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F.核通过E-cadherin/β-Catenin通路增强口腔状细胞癌的扩散
Zhengrui Li1,2,3,4,5,6,7, Yuan Liu1,2,3,4,5,6,7, Xufeng Huang8
1Department of Oral and Maxillofacial-Head and Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, No. 639, Zhizaoju Road, Huangpu District, Shanghai, 200011, China.
BMC oral health
|May 2, 2024
概括
Fusobacterium nucleatum通过激活CDH1/β-catenin通路来促进口腔状细胞癌 (OSCC) 细胞的增殖. 这一发现增强了对OSCC进展的理解,并确定了潜在的治疗点.
科学领域:
- 微生物学 微生物学
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
背景情况:
- 菌核素 (F. nucleatum) 是口腔状细胞癌 (OSCC) 进展的已知危险因素.
- 在此之前,F. nucleatum在促进OSCC细胞增殖方面的特定作用尚不清楚.
研究的目的:
- 为了研究F. nucleatum对OSCC细胞增殖的影响.
- 阐明了F.核诱导的OSCC细胞生长背后的分子机制.
主要方法:
- 实验室细胞培养实验 (CCK-8测定,细胞周期分析) 和体内研究在BALB/c裸体小鼠中进行.
- 研究了F.核,CDH1,β-catenin,cyclinD1和Myc.核之间的相互作用.
- 评估了对非癌细胞的影响,并利用了基因过度表达模型.
主要成果:
- F. nucleatum显著促进OSCC细胞增殖,在72小时内细胞数量翻番,并导致G2/M阶段停止.
- F.核与CDH1的相互作用触发了酸化,导致β-catenin的上调和cyclinD1和Myc.的激活.
- 在体内实验表明,在F. nucleatum干预后,瘤体积和增殖指数 (Ki-67) 增加,但对非癌细胞没有影响.
结论:
- F. nucleatum通过CDH1/β-catenin信号通路促进OSCC细胞的增殖.
- 这项研究加深了对F. nucleatum在OSCC中的致癌作用的理解.
- 鉴定的途径为OSCC治疗提供了潜在的治疗点.
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