Colorectal cancer (CRC) represents a significant global health burden, ranking as the third most common cancer and the second leading cause of cancer-related deaths worldwide. The gut microbiome, composed of trillions of commensal microorganisms, plays a vital role in maintaining homeostasis and overall health. Mounting evidence suggests that alterations in the gut microbiome, referred to as dysbiosis, may contribute to the initiation and progression of CRC by modulating the tumor microenvironment (TME), including the tumor stroma.
Bacteria | Mechanism of Action | References |
---|---|---|
Preliminary Pro-Cancer | ||
Fusobacterium nucleatum | Induces DNA damage and genetic changes, promotes cytokine production, influences immune regulation, possibly enhancing CRC progression. | [23][24][31][32][23,24,31,32] |
Bacteroides fragilis | Produces cytotoxic BFT, alters cellular structures, induces inflammation and activates signaling pathways, triggers changes in host defense mechanisms contributing to CRC. | [33][34][33,34] |
Enterococcus faecalis | Utilizes biliverdin to promote CRC cell proliferation and angiogenesis, induces immunomodulation, causes genomic instability and disrupts intestinal barrier, contributing to CRC progression. | [35][36][35[37],36,37] |
Escherichia coli (phylotype B2, genotoxic pks + E. coli) | Overrepresented cytotoxic phenotype contributes to DNA damage, promotes carcinogenic effects via the production of colibactin mediated by the pks gene. | [38][39][40][38,39,40] |
Peptostreptococcus anaerobius | Adheres to CRC cells via PCWBR2 protein, activates PI3K–Akt–FAK pathway, promotes cell proliferation and triggers pro-inflammatory responses, enhancing CRC progression. | [41][42][41,42] |
Streptococcus gallolyticus | Adheres to host cells via Type VII secretion system, stimulates cell proliferation and promotes CRC via upregulation of β-catenin, c-Myc, and PCNA. | [43][44][45][43,44,45] |
Clostridium septicum | Exacerbates CRC through α-toxin production, induces necrosis and mucosal ulceration, impairs immune response, fostering a conducive environment for CRC. | [46][47][48][46,47,48] |
Preliminary Anti-Cancer | ||
Ruminococcus gnavus | Reduces tumor growth and degrades inhibitory compounds like lyso-glycerophospholipids, enhancing the activity of CD8+ T cells, potentially mitigating CRC progression. | [49][50][49,50] |
Bifidobacterium longum | Modulates oncogenic and tumor suppressor miRNAs, suppresses pro-inflammatory cytokines, enhances adhesion to the intestinal tract, increases short-chain fatty acids production, and improves intestinal barrier function, potentially mitigating CRC progression. | [51][52][53][54][51,52,53,54] |
Lactobacillus acidophilus | Induces apoptosis in CRC cells, mitigates ulcerative colitis via increased acetate production and control of inflammation, potentially reducing CRC progression. | [51][52][55][56][57][51,52,55,56,57] |
Lactobacillus rhamnosus | Triggers apoptosis in cancer cells, boosts immune responses, increases carcinoembryonic antigen secretion from cancer cells, modulates gut immune landscape by increasing CD8 T-cell responses, potentially mitigating CRC progression. | [52][58][59][60][61][52,58,59,60,61] |
Faecalibacterium prausnitzii | Reduces formation of aberrant crypt foci, suppresses lipid peroxidation levels, inhibits CRC cell proliferation, enhances gut microbiota diversity, produces butyrate to augment tumor-suppressing effects, potentially mitigating CRC progression. | [62][63][62,63] |
Bifidobacterium breve | Stimulates immune response by increasing cytotoxic CD8+ T cells, promotes production of anti-tumor cytokines, potentially reducing CRC progression. | [49][64][65][66][49,64,65,66] |
Lactobacillus reuteri | Provokes caspase-9-dependent apoptosis in tumor cells, inhibits cell invasion and proliferation, reduces proliferation and survival in colon cancer cells with its metabolite, reuterin, potentially mitigating CRC progression. | [52][67][68][69][52,67,68,69] |
Bifidobacterium adolescentis | Suppresses colorectal carcinogenesis, inhibits harmful bacterial enzymes such as β-glucuronidase, β-glucosidase, tryptophanase, and urease, differentially regulates Treg/Th17 immune responses, potentially reducing CRC progression. | [52][70][71][72][52,70,71,72] |
Lactobacillus plantarum | Strengthens the intestinal mucosal barrier by regulating occludin and claudin-1 proteins, inhibits harmful bacterial enzymatic activity, regulates CRC cell proliferation and apoptosis, potentially mitigating CRC progression. | [52][73][74][75][52,73,74,75] |