Fig. 2

Hallmarks of cancer influenced my F. nucleatum infection. (1) Production of reactive oxygen species (ROS) and cytokines by F. nucleatum causes DNA damage resulting in genomic instability. (2) F. nucleatum infection in HNSCC causes hypermethylation of CpG islands located in the promoter regions of tumour suppressor genes LXN and SMARCA2 resulting in their inactivation. Downregulation of p27, Ku70 and p53 tumour suppressor genes in OSCC results in weakened cell repair ability and increased cell proliferation. (3) LPS/TLR4 signalling results in cytokine production and NF-κB activation which is responsible for tumour-promoting inflammation. Activation of STAT3 upregulates multiple genes responsible for cell proliferation, invasion and metastasis. Upregulated expression of microRNA-21 promotes proliferation of cancer cells. (4) Fusobacterial FadA binds to E-cadherin resulting in decreased phosphorylation of β-catenin. Subsequently, β-catenin translocates to the nucleus, resulting in cell proliferation with increased expression of oncogenic and inflammatory genes. (5) Fusobacterial Fap2 can protect tumours from immune cell attack by inhibiting T-cells and Natural Killer cells. Figure created with BioRender.com