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Fig. 3 | BMC Microbiology

Fig. 3

From: Oral microbiota and Helicobacter pylori in gastric carcinogenesis: what do we know and where next?

Fig. 3

Oral bacteria can affect the inhibition of cell apoptosis. F. nucleatum modulates numerous anti-apoptotic pathways. As a consequence of TLR activation, bacteria stimulate NF-kB signaling. F. nucleatum activates p38, which results in the MMP-9 and MMP-13 secretion and leads to cancer cell invasion and metastasis. Also, F. nucleatum may induce β-catenin signaling by its LPS and FadA. Stimulating the β-catenin expression and increasing the expression of oncogenes C-myc and cyclin D1 lead to cell proliferation. P. gingivalis LPS may stimulate host response via TLRs (TLR2 and TLR4) and enhance the growth of tumor. Also, P. gingivalis induces anti-apoptotic Jak1/Akt/Stat3 signaling. This bacterium can secrete a NDK enzyme, which cleaves ATP and prevents the proapoptotic P2X7 receptor activation, thus modulating ATP/P2X7-signaling. It also causes cell cycle arrest by manipulating cyclin/CDK activity and reduced levels of p53. TLR: Toll-like receptor, NF- kB: nuclear factor kappa B, p38: Mitogen-activated protein kinase p38, MMPs: matrix metalloproteinases, LPS: lipopolisaccharide, FadA: fusobacterial adhesin/invasin, Jak1: Janus kinase 1, Akt: protein kinase B, Stat3: Signal transducer and activator of transcription 3, Bad: Bcl-2-associated death promoter, CDK: cyclin-dependent kinase, p53: Tumor protein p53, NDK: nucleoside diphosphate kinase, ATP: Adenosine triphosphate, P2X7: Purinergic receptor

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