New advances in oral microbiology and tumor research

Table 1 Oral microbiota in patients with various types of cancer

Types of Cancer	Dominant bacterial community	Mechanism of actions	Ref.
Oral squamous cell carcinoma	Porphyromonas gingivalis	It promotes the proliferation, invasion and tumorigenic properties of human immortalized oral epithelial cells	Guo et al[26]
	Fusobacterium nucleatum	Activation of the Wnt/β-catenin signalling pathway via FadA adhesin binding to E-cadherin to promote tumour cell proliferation and invasion	Li et al[27]
	Streptococcus mutans	Produces acetaldehyde by metabolising sugars, which triggers DNA damage and genomic instability and may promote oral cancer	Pavlova et al[28]
Esophageal cancer	Fusobacterium nucleatum	Similar to OSCC patients, EAC patients had significantly higher abundance of Fusobacterium nucleatum in the oral cavity	Kawasaki et al[30]
	Porphyromonas gingivalis	Similar to OSCC patients, EAC patients had significantly higher abundance of Porphyromonas gingivalis in the oral cavity	Kawasaki et al[30]
	Fusobacterium periodonticum	Promotion of epithelial-mesenchymal transition in esophageal cancer cells by BCT protein	Guo et al[31]
Pancreatic cancer	Porphyromonas gingivalis	Secreted Porphyromonas gingivalis-lipopolysaccharides is recognized by TLR2 and TLR4, activates the NF-κB and MAPK signaling pathways, promotes the release of inflammatory factors, and induces the up-regulated expression of Reg3A/G genes, which contributes to pancreatic cancer development and progression	Hiraki et al[34]
	Aggregatibacter actinomycetemcomitans	Aggregatibacter actinomycetemcomitans abundance is significantly increased in the gingival sulcus of PDAC patients	Ma et al[33]
	Oral microbiota	Possible promotion of pancreatic cancer by mutating the p53 tumor suppressor gene	Wei et al[35], Chen et al[36]

OSCC: Oral squamous cell carcinoma; EAC: Esophageal adenocarcinoma; BCT: Bacterial cell toxin; PDAC: Pancreatic ductal adenocarcinoma.