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附带损害:深入了解使宿主细胞易患癌症的细菌机制。

Collateral damage: insights into bacterial mechanisms that predispose host cells to cancer.

机构信息

Centre d'Immunologie de Marseille-Luminy Parc Scientifique et Technologique de Luminy, Case 906, 13288 Marseille Cedex 09, France.

Unité de Recherche sur les Maladies Infectieuses et Tropicales Émergentes (URMITE), Unités Mixtes de Recherche (UMR) 6236, Faculté de Médecine, 27 Boulevard Jean Moulin, 13385 Marseille Cedex 05, France.

出版信息

Nat Rev Microbiol. 2017 Feb;15(2):109-128. doi: 10.1038/nrmicro.2016.171. Epub 2017 Jan 3.

Abstract

Infections are estimated to contribute to 20% of all human tumours. Viruses are known to induce cell transformation, but evidence has also linked bacteria, such as Helicobacter pylori and Salmonella enterica subsp. enterica serovar Typhi, to different cancer types. In addition, Chlamydia trachomatis, Fusobacterium nucleatum and Bacteroides fragilis are associated with the development of cancer, although a causal relationship has not yet been established. Bacterial effectors such as colibactin and the virulence factor cytotoxin-associated gene A (CagA) can promote cancer directly by influencing host cell signalling cascades, such as the WNT and ataxia-telangiectasia mutated (ATM) pathways, or indirectly by inducing tissue damage and inflammatory responses. In this Review, we discuss how bacterial pathogens interact with host cells to contribute to the development of cancer.

摘要

据估计,感染占所有人类肿瘤的 20%。病毒已被证实可诱导细胞转化,但有证据表明,细菌(如幽门螺杆菌和伤寒沙门氏菌亚种肠道血清型 Typhi)也与不同类型的癌症有关。此外,沙眼衣原体、具核梭杆菌和脆弱拟杆菌也与癌症的发展有关,尽管尚未建立因果关系。细菌效应物,如 colibactin 和毒力因子细胞毒素相关基因 A (CagA),可以通过影响宿主细胞信号级联反应,如 WNT 和共济失调毛细血管扩张突变 (ATM) 途径,直接促进癌症的发生,或者通过诱导组织损伤和炎症反应间接促进癌症的发生。在这篇综述中,我们讨论了细菌病原体如何与宿主细胞相互作用,从而促进癌症的发展。

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