Fig. 2

The main mechanism of F. nucleatum pathogenesis in CRC is illustrated. The adhesion and invasion of  FadA from F. nucleatum to epithelialand endothelial cells of human in pathway 1 can be observed while levels of  inflammatory cytokine (IL-6, IL-8,IL-10, IL-18, TNF-α, and NF- κB) grow in a proinflammatory microenvironment which in turn leads to colorectal tumor progression; FadA interaction with E-cadherin in pathway 2 in epithelial cells leads to  activating of  β-catenin signaling, increasing NF-κB inflammatory gene expression and enhancing tumor cell proliferation. F.nucleatum-infected cells, on the other hand, enhance miRNA expression by Toll-like receptor activation and therefore miRNA release development. F.nucleatum in pathways 3 and 4 reduces the activity of human T cells in a micro-suppressor of the tumor immune system. The interaction between Fap2 from F.nucleatum and the human inhibitor receptor TIGIT in pathway 5 leads to the death of lymphocyte cells of human, resulting in a microenvironment of immunosuppression that increases the progression of CRC