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Review
. 2014 Mar 27;10(3):e1003933.
doi: 10.1371/journal.ppat.1003933. eCollection 2014 Mar.

Oral bacteria and cancer

Sarah E Whitmore  1 , Richard J Lamont  1
Affiliations
Review

Oral bacteria and cancer

Sarah E Whitmore et al. PLoS Pathog. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Interactions between P. gingivalis and epithelial cells that could produce an oncogenic phenotype.
Extracellular P. gingivalis secrete gingipains, which activate Protease Activated Receptor (PAR) leading to promatrix metalloprotease (MMP)-9 production, and they also convert proMMP-9 to mature MMP-9, along with nucleoside diphosphate kinase (NDK), which cleaves ATP and prevents activation of the proapoptotic P2X7 receptor. Intracellular P. gingivalis activate antiapoptotic Jak-Stat signaling and inhibit expression of the p53 tumor suppressor. Additionally, Erk 1/2 and p38 are activated, which also elevates proMMP-9 expression.
Figure 2
Figure 2. Interactions between F. nucleatum and epithelial cells that could produce an oncogenic phenotype.
Binding of the FadA adhesin to E-cadherin activates β-catenin signaling, resulting in activation of genes that control cell survival and proliferation. F. nucleatum also activates several cyclin dependent kinases (CDKs) and p38, which controls the production of matrix metalloproteases MMP-9 and MMP-13.
See this image and copyright information in PMC

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Publication types