Fusobacterium nucleatum Accelerates the Progression of Colitis-Associated Colorectal Cancer by Promoting EMT

Yu, Mi Ra; Kim, Hye Jung; Park, Hae Ryoun

doi:10.3390/cancers12102728

Cited by 47 publications

(39 citation statements)

References 38 publications

(38 reference statements)

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“…Although F. nucleatum is associated with EMT in cancer development 19 , the involvement of p-EMT in F. nucleatum infection remains unclear. Therefore, we examined the involvement of F. nucleatum in the regulation of p-EMT of OSCC.…”

Section: Resultsmentioning

confidence: 99%

“…It recently has been reported that F. nucleatum is associated with EMT in cancer development. F. nucleatum decrease the levels of epithelial marker including E-cadherin and increase the levels of EMT-associated transcription factors including Snail and Slug in colorectal cancer progression 19 . Moreover, ZEB1 level is upregulated by F. nucleatum exposure in oral cancer cells 20 .…”

mentioning

confidence: 95%

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Conversion from epithelial to partial-EMT phenotype by Fusobacterium nucleatum infection promotes invasion of oral cancer cells

Shao

Fujiwara

Mouri

et al. 2021

Sci Rep

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The ability of cancer cells to undergo partial-epithelial mesenchymal transition (p-EMT), rather than complete EMT, poses a higher metastatic risk. Although Fusobacterium nucleatum mainly inhabits in oral cavity, attention has been focused on the F. nucleatum involvement in colorectal cancer development. Here we examined the p-EMT regulation by F. nucleatum in oral squamous cell carcinoma (OSCC) cells. We cultured OSCC cells with epithelial, p-EMT or EMT phenotype with live or heat-inactivated F. nucleatum. Expression of the genes involved in epithelial differentiation, p-EMT and EMT were examined in OSCC cells after co-culture with F. nucleatum by qPCR. Cell growth and invasion of OSCC cells were also examined. Both live and heat-inactivated F. nucleatum upregulated the expression of p-EMT-related genes in OSCC cells with epithelial phenotype, but not with p-EMT or EMT phenotype. Moreover, F. nucleatum promoted invasion of OSCC cells with epithelial phenotype. Co-culture with other strains of bacteria other than Porphyromonas gingivalis did not alter p-EMT-related genes in OSCC cells with epithelial phenotype. F. nucleatum infection may convert epithelial to p-EMT phenotype via altering gene expression in OSCC. Oral hygiene managements against F. nucleatum infection may contribute to reduce the risk for an increase in metastatic ability of OSCC.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 95%

Conversion from epithelial to partial-EMT phenotype by Fusobacterium nucleatum infection promotes invasion of oral cancer cells

Shao

Fujiwara

Mouri

et al. 2021

Sci Rep

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“…In sporadic CRC, Fusobacterium nucleatum, through the expression of virulence factors that confer the capacity to adhere to epithelial cells and to induce the activation of the beta-Catenin and Wnt pathways, has been shown to promote cancer development (extensively reviewed in Brennan and Garrett 2019 [106] ). Recently, F. nucleatum has also been shown to worsen tumor induction in the AOM/DSS model of CAC by activating EGFR signaling pathways and promoting epithelial-to-mesenchymal transition, a key event in colon carcinogenesis [107] . The enterotoxigen Bacteroides fragilis has been shown to induce colitis and to pro-mote tumorigenesis in APC min/ + mice.…”

Section: Role Of Intestinal Microbiota In Cacmentioning

confidence: 99%

From inflammation to colitis-associated colorectal cancer in inflammatory bowel disease: Pathogenesis and impact of current therapies

Fantini

Guadagni

2021

Digestive and Liver Disease

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The risk of colorectal cancer (CRC) is higher in patients with inflammatory bowel disease (IBD). Population-based data from patients with ulcerative colitis (UC) estimate that the risk of CRC is approximately 2-to 3-fold that of the general population; patients with Crohn's disease appear to have a similar increased risk. However, the true extent of colitis-associated cancer (CAC) in undertreated IBD is unclear. Data suggest that the size (i.e., severity and extent) and persistence of the inflammatory process is largely responsible for the development of CRC in IBD. As patients with IBD and CRC have a worse prognosis than those without a history of IBD, the impact of current therapies for IBD on CAC is of importance. Chronic inflammation of the gut has been shown to increase the risk of developing CAC in both UC and CD. Therefore, control of inflammation is pivotal to the prevention of CAC. This review presents an overview of the current knowledge of CAC in IBD patients, focusing on the role of inflammation in the pathogenesis of CAC and the potential for IBD drugs to interfere with the process of carcinogenesis by reducing the inflammatory process or by modulating pathways directly involved in carcinogenesis.

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“…et al suggested that F. nucleatum well promotes epithelial to mesenchymal transition during colon cancer progression [ 24 ]. Using the cancer cell line and the AOM-DSS model of colitis-associated colon cancer, this group demonstrated that when used with epithelial barrier disruptive agent DSS, F. nucleatum synergistically increased the aggressiveness and EMT characteristics of cancer cells and this process involved EGFR signaling pathways [ 24 ]. Finally, the impact of the microbiome on the human epigenome was recently nicely overviewed by Dr. J. Allet and Dr. C. Sears [ 25 ].…”

Section: Mechanistic Links Between Microbiota and Colon Cancermentioning

confidence: 99%

Drug–Microbiota Interaction in Colon Cancer Therapy: Impact of Antibiotics

et al. 2021

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Colon adenocarcinoma is one of the most common malignancies, and it is highly lethal. Chemotherapy plays an important role in the treatment of colon cancer at various stages of the disease. The gut microbiome has emerged as a key player in colon cancer development and progression, and it can also alter the therapeutic agent’s efficacy and toxicities. Antibiotics can directly and/or indirectly affect the balance of the gut microbiome and, therefore, the clinical outcomes. In this article, we provided an overview of the composition of the gut microbiome under homeostasis and the mechanistic links between gut microbiota and colon cancer. The relationship between the use of oral antibiotics and colon cancer, as well as the impact of the gut microbiome on the efficacy and toxicities of chemotherapy in colon cancer, are discussed. Potential interventions to modulate microbiota and improve chemotherapy outcomes are discussed. Further studies are indicated to address these key gaps in the field and provide a scientific basis for the design of novel microbiota-based approaches for prevention/use as adjuvant therapeutics for patients with colon cancer.

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Fusobacterium nucleatum Accelerates the Progression of Colitis-Associated Colorectal Cancer by Promoting EMT

Cited by 47 publications

References 38 publications

Conversion from epithelial to partial-EMT phenotype by Fusobacterium nucleatum infection promotes invasion of oral cancer cells

Conversion from epithelial to partial-EMT phenotype by Fusobacterium nucleatum infection promotes invasion of oral cancer cells

From inflammation to colitis-associated colorectal cancer in inflammatory bowel disease: Pathogenesis and impact of current therapies

Drug–Microbiota Interaction in Colon Cancer Therapy: Impact of Antibiotics

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