具核梭杆菌促进结直肠癌发生发展机制的研究进展  

Research progress on the mechanism of Fusobacterium nucleatum promoting the initiation and development of colorectal cancer

作　　者：罗婉逸 韩居熺 周学东[1,2] 彭显[1,2] 郑欣 Luo Wanyi;Han Juxi;Zhou Xuedong;Peng Xian;Zheng Xin(State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&West China School of Stomatology,Sichuan University,Chengdu 610041,China;State Key Laboratory of Oral Diseases&National Clinical Research Center for Oral Diseases&Dept.of Cariology and Endodontics,West China Hospital of Stomatology,Sichuan University,Chengdu 610041,China)

机构地区：[1]口腔疾病研究国家重点实验室,国家口腔疾病临床医学研究中心,四川大学华西口腔医学院,成都610041 [2]口腔疾病研究国家重点实验室,国家口腔疾病临床医学研究中心,四川大学华西口腔医院牙体牙髓病科,成都610041

出　　处：《国际口腔医学杂志》2023年第1期52-60,共9页International Journal of Stomatology

基　　金：四川大学华西口腔医院人才队伍建设科研经费(RCDWJS2020-11)。

摘　　要：具核梭杆菌是一种革兰阴性厌氧菌,广泛定植于人体口腔内,是公认的牙周致病菌。该菌不仅在牙周病、口腔癌等口腔疾病中起着重要作用,还与全身各系统多种疾病存在关系,包括心血管疾病、骨关节炎、妊娠不良事件及各系统肿瘤。具核梭杆菌与结直肠癌的关系是当前研究的热点问题。存在肠道炎症的患者,牙周炎或可成为一个促进炎症向癌症转变的风险因素。具核梭杆菌可通过消化道及血液循环两条途径迁移到肠道,进一步通过黏附素-上皮细胞钙黏蛋白和黏附素-糖类肿瘤标记物两条途径与结直肠癌细胞特异性结合。具核梭杆菌对肿瘤内乏氧的高代谢环境具有较强的适应能力,可进一步促进肿瘤的糖酵解,互利共生的关系使得具核梭杆菌在肿瘤中大量富集。与结直肠癌细胞结合后,具核梭杆菌通过调控经典Wnt信号通、核因子κB等信号通路,改变免疫微环境,促进肿瘤的生长和转移,并表现出抗化学治疗的作用,对结直肠癌的发生发展和治疗造成影响。Fusobacterium nucleatum(F. nucleatum) is a Gram-negative anaerobic bacterium that widely colonizes the human oral cavity and is recognized as a periodontal pathogen. F. nucleatum plays an important role in oral diseases, such as periodontal disease and oral cancer, and is biologically associated with a variety of systematic diseases, including cardiovascular disease, alveolar bone loss, adverse pregnancy outcomes, and cancers of various systems. The correlation between F. nucleatum and colorectal cancer(CRC) is well documented. We conclude that periodontitis may be a risk factor for inflammatory transition to cancer in patients with intestinal inflammation. F. nucleatum migrates to the intestine through the digestive tract and blood circulation and binds specifically to CRC cells via the adhesin FadA/Ecadherin and adhesin Fap2/disaccharide tumor marker in gal-GalNac pathways. F. nucleatum can adapt to the highly metabolic, oxygen-lacking environment of tumors and further promote the glycolysis of tumors, which leads to the high abundance of F. nucleatum in CRC. By binding to CRC cells, F. nucleatum regulates canonical Wnt/β-catenin pathway and nuclear factor kappa-B signaling pathways, thus promoting the initiation, metastasis, and chemoresistance of cancer cells and affecting the tumor immune microenvironment.

关 键 词：具核梭杆菌 结直肠癌 肿瘤免疫微环境 

分 类 号：R780.2[医药卫生—口腔医学]