Fig. 2
Main effects of individual members of the oral microbiota on hallmarks of cancer. Selected examples of oral microbiota and their molecular mechanisms are shown to be modulating each of the cancer hallmarks, including sustaining proliferative signaling (a), evading growth suppressors (b), resisting cell death (c), enabling replicative immortality (d), activating invasion and metastasis (e), reprogramming of energy metabolism (f), promoting genome instability (g), inducing angiogenesis (h), inducing tumor-promoting inflammation (i), and evading immune destruction (j). DSBs double-strand breaks, ERK extracellular regulated protein kinases, F. nucleatum Fusobacterium nucleatum, H2S hydrogen sulfide, LPS lipopolysaccharide, miR-21 MicroRNA 21, MMP-9 matrix metalloproteinase-9, MSI microsatellite instability, OMP outer membrane protein, OMVs outer membrane vesicles, OXPHOS oxidative phosphorylation, P. gingivalis Porphyromonas gingivalis, PAD peptidyl arginine deaminase, PI3K phosphatidylinositol 3-kinase, Sp1 specificity protein 1, TCF transcription factor, TERT telomerase reverse transcriptase, TIGIT T cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain, TLR4 toll-like receptor 4, VEGF-A vascular endothelial growth factor-A