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具核梭杆菌的致癌机制

Carcinogenesis mechanisms of Fusobacterium nucleatum.

作者信息

Gholizadeh Pourya, Eslami Hosein, Kafil Hossein Samadi

机构信息

Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.

Dental and Periodontal Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

Biomed Pharmacother. 2017 May;89:918-925. doi: 10.1016/j.biopha.2017.02.102. Epub 2017 Mar 7.

Abstract

Transformed cells of cancers may be related to stromal cells, immune cells, and some bacteria such as Fusobacterium nucleatum. This review aimed to evaluate carcinogenesis mechanisms of Fusobacterium spp. in the oral cavity, pancreatic and colorectal cancers. These cancers are the three of the ten most prevalence cancer in the worldwide. Recent findings demonstrated that F. nucleatum could be considered as the risk factor for these cancers. The most important carcinogenesis mechanisms of F. nucleatum are chronic infection, interaction of cell surface molecules of these bacteria with immune system and stromal cells, immune evasion and immune suppression. However, there are some uncertainty carcinogenesis mechanisms about these bacteria, but this review evaluates almost all the known mechanisms. Well-characterized virulence factors of F. nucleatum such as FadA, Fap2, LPS and cell wall extracts may act as effector molecules in the shift of normal epithelial cells to tumor cells. These molecules may provide new targets, drugs, and strategies for therapeutic intervention.

摘要

癌症的转化细胞可能与基质细胞、免疫细胞以及一些细菌(如具核梭杆菌)有关。本综述旨在评估梭杆菌属在口腔癌、胰腺癌和结直肠癌中的致癌机制。这些癌症是全球十大最常见癌症中的三种。最近的研究结果表明,具核梭杆菌可被视为这些癌症的危险因素。具核梭杆菌最重要的致癌机制是慢性感染、这些细菌的细胞表面分子与免疫系统和基质细胞的相互作用、免疫逃逸和免疫抑制。然而,关于这些细菌的致癌机制仍存在一些不确定性,但本综述评估了几乎所有已知机制。具核梭杆菌特征明确的毒力因子,如FadA、Fap2、脂多糖和细胞壁提取物,可能在正常上皮细胞向肿瘤细胞的转变中充当效应分子。这些分子可能为治疗干预提供新的靶点、药物和策略。

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