Breast cancer is among the most prevalent malignancies in women worldwide. Epidemiological findings suggested that periodontal diseases may be associated with breast cancer, among which Fusobacterium nucleatum is considered an important cross-participant. In this work, we comprehensively summarize the known mechanisms of how F. nucleatum translocates to, colonizes in mammary tumors, and promotes the carcinogenesis. Specifically, F. nucleatum translocates to mammary tissue through the mammary–intestinal axis, direct nipple contact, and hematogenous transmission. Subsequently, F. nucleatum takes advantage of fusobacterium autotransporter protein 2 to colonize breast cancer and uses virulence factors fusobacterium adhesin A and lipopolysaccharide to promote proliferation. Moreover, the upregulated matrix metalloproteinase-9 induced by F. nucleatum does not only trigger the inflammatory response but also facilitates the tumor-promoting microenvironment. Aside from the pro-inflammatory effect, F. nucleatum may also be engaged in tumor immune evasion, which is achieved through the action of virulence factors on immune checkpoint receptors highly expressed on T cells, natural killer cells, and tumor-infiltrating lymphocytes. Taking breast cancer as an example, more relevant research studies may expand our current knowledge of how oral microbes affect systemic health. Hopefully, exploring these mechanisms in depth could provide new strategies for safer and more effective biologic and targeted therapies targeted at breast cancer.

中文翻译：

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具核梭杆菌易位至乳腺组织并促进乳腺癌发展的方式

乳腺癌是全世界女性最常见的恶性肿瘤之一。流行病学研究结果表明，牙周病可能与乳腺癌有关，其中具核梭杆菌被认为是重要的交叉参与者。在这项工作中，我们全面总结了具核梭菌在乳腺肿瘤中易位、定植和促进癌变的已知机制。具体来说，具核梭杆菌通过乳肠轴、直接乳头接触和血行传播转移到乳腺组织。随后，具核梭杆菌利用梭杆菌自转运蛋白2定植乳腺癌，并利用毒力因子梭杆菌粘附素A和脂多糖促进增殖。此外，具核梭杆菌诱导的基质金属蛋白酶9上调不仅能引发炎症反应，还能促进促肿瘤微环境的形成。除了促炎作用外，具核梭菌还可能参与肿瘤免疫逃避，这是通过毒力因子作用于 T 细胞、自然杀伤细胞和肿瘤浸润淋巴细胞上高表达的免疫检查点受体来实现的。以乳腺癌为例，更多相关研究可能会扩大我们目前对口腔微生物如何影响全身健康的认识。希望深入探索这些机制可以为针对乳腺癌的更安全、更有效的生物和靶向治疗提供新策略。