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Table 1 Intratumoural microbiota in different cancer tissues and their role in cancer tumorigenesis, progression and prognosis

From: Intratumoural microbiota: from theory to clinical application

Cancer

Status

Intratumoural microbiota

Mechanism

References

Breast cancer

Higher content

Fusobacterium nucleatum

1. Causes cancer

2. leads to poor prognosis by suppressing the immune response

[11]

Reduction

Anaerococcus, Streptococcus, Propionibacterium

1. negatively correlated with carcinogenic immune characteristics

2. Positively correlated with T-cell activation-related genes

[12]

Ovarian cancer

Content increasing

Brucella, Chlamydia, Mycoplasma

Progressive chromosome loss and translocations cause chromosomal changes and in vitro cell transformation, promoting tumor formation

[13]

Prostate cancer

Higher content

Pseudomonas, Escherichia, Immunobacterium,

Propionibacterium spp.

Induces prostatitis, enhances differentiation of prostate basal cells into ductal cells and promotes tumor formation

[14]

Bacillus deformans

Induces prostatitis and promotes tumor formation

[15]

Propionibacterium acnes spp.

By forming inflammation of the prostate tissue, which in turn leads to the formation of tumors

[16]

Content increasing

Staphylococcus

Induce inflammation of the prostate tissue and promotes tumor formation

[15]

Colorectal cancer

Higher content

F. nucleic acids

1. F. nucleatum adhesion molecules bind to cell surface motifs on cancer or immune cells, resulting in downstream oncogenic or immunosuppressive signaling

2. Activation of beta-linked protein signaling;

3. resulting in low CD3 T cell density;

4. causes NK and T cell inactivation

[9] [17]

E.coli expressing genomic island polyketide synthase (pks + E.coli)

pks + E.coli-derived alkylation of DNA by E.coli and production of DNA adducts that lead to DNA damage in colonic epithelial cells and ultimately promote cancer development

[18]

Enterotoxin-producing

Bacteroides fragilis (ETBF)

ETBF promotes cancer development by recruiting other bacteria and immune cells to the tumor site and promoting IL-17-mediated inflammation

[19]

Fusobacterium

1. Enhances tumor cell adhesion and invasion 2. regulation of host immune response 3. Activates Toll-like receptor 4 pathway

[17]

Presence

Bifidobacterium

Local delivery of bifidobacteria effectively stimulates STING signaling and increases crossover initiation of dendritic cells following anti-CD47 treatment, thereby influencing treatment

[20]

Pancreatic cancer

Higher content

Enterobacteriaceae,

Pseudomonas spp.

Regulates metabolism of chemotherapeutic drugs, leading to chemoresistance and ultimately affecting the efficacy of treatment

[21] [22]

Mycobacterium avium

Influences tumor progression by regulating M1 macrophage/Th1 differentiation that affects CD8 + T cell function

[22]

Pseudoxanthomonas,

Streptomyces, sucrose

polyspora, Bacillus cereus

Elevates CD8 T-cell infiltration and activation, affecting prognosis

[22]

Malassezia globosa

Promotes tumorigenesis, tumor growth and gemcitabine resistance through the mannose-binding lectin C3 axis, thereby influencing tumor formation, progression, and prognosis

[23]

Lung Cancer

Higher content

Acidovorax spp.

Associated with TP53 mutations

[24]

Legionella

Affects metastasis of cancer

[25]

Esophageal cancer

Higher content

Lactobacillus fermentum

Can be used for cancer screening

[26]

Campylobacter spp.

Causes inflammation and affects the prognosis of the tumor

[27]

F. nucleic acids

As a prognostic biomarker

[28]

Porphyromonas gingivalis

1. Promotes immune evasion of tumor cells 2. Inhibits apoptosis of epithelial cells

[29]

Fusobacterium nucleatum

Promote tumor invasion of Treg lymphocytes in a chemokine (especially CCL20) dependent manner, promote aggressive tumor behavior, and affect tumor progression

[30]

Ecological

disorders

Fusobacterium nucleatum, Streptococcus oligosporus

Confer chemoresistance to ESCC cells through modulation of autophagy

[30]

Stomach Cancer

Higher content

Helicobacter pylori

Enhance tumor formation by promoting p53 degradation and immune escape

[31]

Bladder Cancer

Higher content

E.coli, butyrate-producing bacteria, oscillating bacilli

Associates with EMT-related genes, leading to poor prognosis

[32]

Oral cancer

Higher content

Fusobacterium nucleatum

Facilitates EMT transition and can be used to predict

[33]

Fusobacterium nucleatum, Prevotella

Causes different types of pulp infections and promotes tumor formation

[33]

Streptococcus peptidis

Enhances anti-tumor immune response and promotes tumor prognosis

[34]

Ecological disorders

Mucor (especially Streptococcus), Actinomyces (especially Rhodococcus)

Promotes cancer and progression

[35]

Cervical cancer

Higher content

Fusobacterium spp.

FadA gene overexpression promotes tumor formation

[36]

L. crispatus, L. iners

Promotes tumor formation

[36]

Ecological

disorders

Lactobacillus lactis,

Serratia marcescens

Raising vaginal pH and promoting tumor formation

[37]

Endometrial cancer

Higher content

Atopobium, Porphyromonas

Dialister, Peptoniphilus

Ruminococcus,

Anaerotruncus

Anaerostipes, Treponema

Bacteroides, Arthrospira

Regulates vaginal pH and promotes tumor formation

[37]

Liver cancer

Higher content

Helicobacter bifidus

Induces chronic hepatitis and promotes tumor formation

[38]

Extrahepatic bile duct cancer

Content increasing

Methanobacterium,

Fusobacterium, Prevotella, Actinomyces, Neosynovia, H. pylori H

Increases cagA and vacA gene abundance and promotes tumor formation

[39]

Reduction

Helicobacter bilis

Induces inflammation and promotes tumor formation

[40]

Bile duct cancer

Higher content

Bifidobacteriaceae,

Enterobacteriaceae,

Enterococcaceae

Metabolic activities can lead to the formation of carcinogens, such as ammonia and bile acids, which promote tumor formation

[41]

Gallbladder cancer

Higher content

Fusobacterium nucleatum, Escherichia coli,

Enterobacter spp.

Promotes the development of gallstones and chronic cholecystitis, which in turn promotes the formation of tumors

[42]