Carcinogenesis mechanisms of Fusobacterium nucleatum

被引:125
|
作者
Gholizadeh, Pourya [1 ,2 ]
Eslami, Hosein [3 ]
Kafil, Hossein Samadi [4 ,5 ]
机构
[1] Tabriz Univ Med Sci, Hematol & Oncol Res Ctr, Tabriz, Iran
[2] Tabriz Univ Med Sci, Student Res Comm, Tabriz, Iran
[3] Tabriz Univ Med Sci, Dent & Periodontal Res Ctr, Tabriz, Iran
[4] Tabriz Univ Med Sci, Infect & Trop Med Res Ctr, Tabriz, Iran
[5] Tabriz Univ Med Sci, Drug Appl Res Ctr, Tabriz, Iran
关键词
Fusobacterium nucleatum; Mechanisms; Oral cavity cancer; Pancreatic cancer; Colorectal cancer; MELANOMA INHIBITORY-ACTIVITY; GINGIVAL EPITHELIAL-CELLS; MOBILITY GROUP BOX-1; TUMOR PROGRESSION; ORAL-CANCER; RECEPTOR; IMMUNE; ACTIVATION; INFECTION; FADA;
D O I
10.1016/j.biopha.2017.02.102
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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. (C) 2017 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:918 / 925
页数:8
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