Fusobacterium nucleatum, a gram-negative anaerobic bacterium, has emerged as a significant player in colorectal cancer (CRC) pathogenesis. The bacterium causes a persistent inflammatory reaction in the colorectal mucosa by stimulating the release of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, creating an environment conducive to cancer progression.F. nucleatumbinds to and penetrates epithelial cells through adhesins such as FadA, impairing cell junctions and encouraging epithelial-to-mesenchymal transition (EMT), which is associated with cancer advancement. Additionally, the bacterium modulates the host immune system, suppressing immune cell activity and creating conditions favorable for tumor growth. Its interactions with the gut microbiome contribute to dysbiosis, further influencing carcinogenic pathways. Evidence indicates thatF. nucleatumcan inflict DNA damage either directly via reactive oxygen species or indirectly by creating a pro-inflammatory environment. Additionally, it triggers oncogenic pathways, especially the Wnt/β-catenin signaling pathway, which promotes tumor cell growth and longevity. Moreover,F. nucleatumalters the tumor microenvironment, impacting cancer cell behavior, metastasis, and therapeutic responses. The purpose of this review is to elucidate the molecular mechanisms by whichF. nucleatumcontributes to CRC. Understanding these mechanisms is crucial for the development of targeted therapies and diagnostic strategies for CRC associated withF. nucleatum.
具核梭杆菌是一种革兰阴性厌氧菌，在结直肠癌发病机制中扮演重要角色。该菌通过刺激促炎细胞因子（如IL-1β、IL-6和TNF-α）的释放，在结直肠黏膜引发持续性炎症反应，从而形成有利于癌症进展的微环境。具核梭杆菌通过FadA等黏附素与上皮细胞结合并穿透细胞，破坏细胞连接并促进上皮-间质转化，这一过程与癌症发展密切相关。此外，该菌可调控宿主免疫系统，抑制免疫细胞活性，为肿瘤生长创造有利条件。其与肠道微生物组的相互作用导致菌群失调，进一步影响致癌通路。研究表明，具核梭杆菌可通过活性氧直接造成DNA损伤，或通过促炎环境间接导致DNA损伤。同时，它能激活致癌通路（特别是Wnt/β-catenin信号通路），促进肿瘤细胞增殖与存活。该菌还能改变肿瘤微环境，影响癌细胞行为、转移过程及治疗反应。本综述旨在阐明具核梭杆菌促进结直肠癌发展的分子机制，深入理解这些机制对于开发针对具核梭杆菌相关结直肠癌的靶向治疗和诊断策略具有重要意义。
肿瘤(癌症)患者之家