Table 1.
Summary of pro-metastatic microbiome findings.
| Microbiome or Microbial Metabolites |
Cancer Type | Impact on Metastasis * |
Mechanism | In Vivo/In Vitro | Refs. |
|---|---|---|---|---|---|
| Fusobacterium nucleatum | CRC | ↑ | Increases CYP2J2 and 12,13-EpOME (oncogenic metabolites) by activating the TLR4/Keap1/NRF2 axis, thereby promoting EMT | Both | [45] |
| Fusobacterium nucleatum | CRC | ↑ | Modulates E-Cadherin/β-Catenin signaling via its FadA adhesin and further activates the Wnt signaling pathway, leading to enhanced EMT |
Both | [29] |
| Fusobacterium nucleatum | laryngeal squamous cell cancer (LSCC) | ↑ | Increases miR-155-5p and miR-205-5p expression to suppress ADH1B and TGFBR2 expression, leading to reprogramming of ethanol metabolism to allow Fn accumulation and PI3K/AKT signaling pathway activation to promote EMT | Both | [46] |
| Porphyromonas gingivalis | oral squamous cell carcinoma (OSCC) | ↑ | Downregulates nucleoplasmic accumulation of E-calmodulin and β-linked protein to promote EMT | In vitro | [47] |
| T epidimonas fonticaldi | pancreatic ductal adenocarcinoma (PDAC) | ↑ | EMT-related mRNA and TCA cycle-related metabolites are significantly increased | In vitro | [48] |
| Fusobacterium nucleatum | Breast cancer | ↑ | Inhibits the killing of cancer cells by NK cells and tumor-infiltrating T cells and the accumulation of tumor-infiltrating T cells | Both | [10] |
| Fusobacterium nucleatum | CRC | ↑ | Lowers the density of CD8+ T cells and increases the density of MDSCs | In vitro | [49] |
| Staphylococcus aureus | PC | ↑ | Activates regulatory T cells, which suppress the activation and proliferation of effector T cells and impair the immune system | In vitro | [25] |
| gut microbes | melanoma | ↑ | Inhibits the growth of bone marrow NK and Th1 cells by blocking the S1P-S1PR1/5 axis and CXCR3-CXCL9 chemokine gradient | In vivo | [50] |
| Escherichia coli | CRC | ↑ | Causes CTSK overexpression, TLR4, to stimulate M2 polarization of TAMs and secretion of cytokines, including IL10 and IL17 through the motor-dependent pathway, which, in turn, promotes invasive metastasis of CRC cells through the NF-κβ pathway | Both | [25] |
| Fusobacterium nucleatum | CRC | ↑ | Promotes CRC metastasis through miR-1322/CCL20 axisand M2 polarization | Both | [51] |
| Trichomonas vaginalis | PC | ↑ | Secretes the pro-inflammatory cytokine IL-6, which drives M2 polarization | In vitro | [52] |
| Staphylococcus xylosus, Lactobacillus animalis, and Streptococcus cuniculi | breast cancer | ↑ | Enhances resistance to FSS by reorganizing the actin cytoskeleton | Both | [4] |
| oral pathogens | OSCC | ↑ | Causes TLR signaling, which in turn causes IL-6 production and STAT3 activation. Then, it activates essential effectors, including cyclinD1, MMP-9, and heparinase | Both | [30] |
| Porphyromonas gingivalis | OSCC | ↑ | Stimulates MMP-1 and MMP-10 through the release of IL-8 and gingival protease | In vitro | [41] |
| Epstein-Barr virus | Head and neck squamous cell carcinomas | ↑ | Decreases the stability of p53 and increases the secretion of MMPs | In vitro | [53] |
* ↑ microbes promote cancer metastasis.