Involvement of Fusobacterium Species in Oral Cancer Progression: A Literature Review Including Other Types of Cancer

Abstract

Chronic inflammation caused by infections has been suggested to be one of the most important cause of cancers. It has recently been shown that there is correlation between intestinal bacteria and cancer development including metastasis. As over 700 bacterial species exist in an oral cavity, it has been concerning that bacterial infection may cause oral cancer. However, the role of bacteria regarding tumorigenesis of oral cancer remains unclear. Several papers have shown that Fusobacterium species deriving the oral cavities, especially, play a crucial role for the development of colorectal and esophageal cancer. F. nucleatum is a well-known oral bacterium involved in formation of typical dental plaque on human teeth and causing periodontal diseases. The greatest characteristic of F. nucleatum is its ability to adhere to various bacteria and host cells. Interestingly, F. nucleatum is frequently detected in oral cancer tissues. Moreover, detection of F. nucleatum is correlated with the clinical stage of oral cancer. Although the detailed mechanism is still unclear, Fusobacterium species have been suggested to be associated with cell adhesion, tumorigenesis, epithelial-to-mesenchymal transition, inflammasomes, cell cycle, etc. in oral cancer. In this review, we introduce the reports focused on the association of Fusobacterium species with cancer development and progression including oral, esophageal, and colon cancers.

Keywords: Fusobacterium nucleatum; cancer development and progression; oral cancer.

Figure 1

Schematic model for the involvement of Fusobacterium species in oral carcinogenesis and cancer progression. In a dental plaque, various bacteria exist as shown in the pyramid. The base of the pyramid is comprised of species thought to colonize the tooth surface and proliferate at an early stage. Then, complex species in the middle of pyramid becomes numerically more dominant later and is thought to bridge the early colonizers. Finally, the complex species in the top of the pyramid numerically more dominant at late stages in plaque development. Among them, Fusobacterium species may adhere with oral keratinocyte or oral cancer cells via interaction between FadA/Fap2 and E-cadherin. This interaction may induce carcinogenesis and cancer progression.