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. 2022 Jun 30;13:919633. doi: 10.3389/fmicb.2022.919633

Figure 3.

Figure 3

The synergistic and antagonistic effects among oral bacteria in oral cancer. P. gingivalis and F. nucleatum triggers TLR signaling, resulting in IL-6 production that activates STAT3 which in turn induces oral cancer growth and invasiveness. P. gingivalis can localize FOXO1 in nuclear to promote oral cancer, while the presence of S. gordonii can activate the TAK1-NLK1 pathway, which supersedes the effect of P. gingivalis and translocates FOXO1 to the cytoplasm, where it is inactive. L. plantarum can inhibit oral cancer through upregulation of PTEN and downregulation of MAPK pathways, and its bacteriocin PLNC8 αβ can suppress P. gingivalis growth and subsequent pathogenicity.