Carcinogenesis mechanisms of Fusobacterium nucleatum

Gholizadeh, Pourya; Eslami, Hosein; Kafil, Hossein Samadi

doi:10.1016/j.biopha.2017.02.102

Cited by 138 publications

(122 citation statements)

References 122 publications

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Section: Discussionmentioning

confidence: 99%

“…In humans, some Fusobacterium spp., including Fusobacterium nucleatum, have been associated with an increased risk for colorectal and pancreatic cancers, as well as some oral squamous cell carcinomas. 38,42,44,52 Fusobacterium nucleatum numbers are significantly correlated with tumor size, and shortened survival times in a population of human Japanese patients with later stage CRC compared to earlier stages. 53 These findings, as well as additional observations in rodent models and humans with CRC suggest that chronic inflammatory disease of the GI tract is a potential risk factor for the development of additional channels for amplified inflammatory processes, aneuploidy, high-grade dysplasia, metaplasia and loss of cellular proliferative checkpoints, all of which are processes that can be appreciated in malignancy.…”

Section: Discussionmentioning

confidence: 99%

“…is pro-inflammatory, exhibits adhesive and invasive properties via virulence factors (i.e., FadA, fusobacterium autotransporter protein 2 and fusobacterial outer membrane protein A), and promotes pro-oncogenic features which might contribute to accelerated tumor growth and tumor burden. 38,47,54 Increased Fusobacterium nucleatum is associated with an increase in adenoma formation and accelerated small intestinal adenocarcinoma development in rodent models of GI neoplasia. 41 Coupled with this was an expansion of CD11b + myeloid cells (i.e., dendritic cells, macrophages, and myeloid-derived suppressor cells) in the neoplastic tissues and an NF-κB-driven pro-inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

“…This probe array was selected to identify specific bacterial groups and individual bacterial species previously shown to be relevant in the pathogenesis of intestinal cancers in humans, rodents, and dogs. 9,14,19,22,23,27,[35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54] Tissue sections were bathed in 30μL of DNA-probe-hybridization buffer mix in a hybridization chamber maintained at 54 C overnight (12 hours). Buffer 1 (20mM Tris, 0.9M NaCl, 0.1% SDS, 20% Formamide, 10% Dextran sulfate) was used for the hybridization of Eub338, Erec482, Bacto1080, Fuso0664, Ebac1790 and Faecali698.…”

Section: Fluorescence In Situ Hybridization (Fish)mentioning

confidence: 99%

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Relationship of the mucosal microbiota to gastrointestinal inflammation and small cell intestinal lymphoma in cats

Garraway

Johannes

Bryan

et al. 2018

Veterinary Internal Medicne

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BackgroundThe gastrointestinal (GI) microbiota in healthy cats is altered in IBD. Little research has been performed to identify whether specific bacterial groups are associated with small cell GI lymphoma (LSA).HypothesisMucosal bacteria, including Enterobacteriaceae and Fusobacterium spp., are abundant in intestinal biopsies of cats with small cell GI LSA compared to cats with IBD.AnimalsFourteen cats with IBD and 14 cats with small cell GI LSA.MethodsRetrospective case control study. A search of the medical records was performed to identify cats diagnosed with IBD and with GI LSA. Bacterial groups identified by FISH in GI biopsies were compared between cohorts and correlated to CD11b+ and NF‐κB expression.Results Fusobacterium spp. (median; IQR bacteria/region) were higher in cats with small cell GI LSA in ileal (527; 455.5 – 661.5; P = .046) and colonic (404.5; 328.8 – 455.5; P = .016) adherent mucus, and combined colonic compartments (free mucus, adherent mucus, attaching to epithelium) (8; 0 – 336; P = .017) compared to cats with IBD (ileum: 67; 31.5 – 259; colon: 142.5; 82.3 – 434.5; combined: 3; 0 – 34). Bacteroides spp. were higher in ileal adherent mucus (P = .036) and 3 combined ileal compartments (P = .034) of cats with small cell GI LSA. There were significant correlations between Fusobacterium spp. totals and CD11b+ cell (P = .009; rs .476) and NF‐κB expression (P = .004; rs .523).ConclusionsThe bacterial alterations appreciated might be influential in development of small cell GI LSA, and should drive further studies to elucidate the effects of microbial‐mediated inflammation on GI cancer progression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Fluorescence In Situ Hybridization (Fish)mentioning

confidence: 99%

See 2 more Smart Citations

Relationship of the mucosal microbiota to gastrointestinal inflammation and small cell intestinal lymphoma in cats

Garraway

Johannes

Bryan

et al. 2018

Veterinary Internal Medicne

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“…Abed et al showed that F. nucleatum Fap-2 attaches to beta-D-galactosyl(1-3)-N-acetyl-D-galactosamine (Gal-GalNAc) as a polysaccharide receptor for CRC, reducing the ability of F. nucleatum to enhance CRC. 98 T Cell immunoreceptor with Ig and ITIM domains (TIGIT) is an important inhibitory receptor on NK and T cells. 99 Gur et al proved that Fap-2 binds to TIGIT on NK and T cells and interferes with the attack by the host immune system on F. nucleatum-associated tumors.…”

Section: Fusobacterium Nucleatummentioning

confidence: 99%

The role of microbiota in the development of colorectal cancer

Dai

Zhang

et al. 2019

Intl Journal of Cancer

104

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Colorectal cancer is the third largest cancer in worldwide and has been proven to be closely related to the intestinal microbiota. Many reports and clinical studies have shown that intestinal microbial behavior may lead to pathological changes in the host intestines. The changes can be divided into epigenetic changes and carcinogenic changes at the gene level, which ultimately promote the production and development of colorectal cancer. This article reviews the pathways of microbial signaling in the intestinal epithelial barrier, the role of microbiota in inflammatory colorectal tumors, and typical microbial carcinogenesis. Finally, by gaining a deeper understanding of the intestinal microbiota, we hope to achieve the goal of treating colorectal cancer using current microbiota technologies, such as fecal microbiological transplantation.

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Harness the functions of gut microbiome in tumorigenesis for cancer treatment

Lee

2021

Cancer Communications

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It has been shown that gut microbiota dysbiosis leads to physiological changes and links to a number of diseases, including cancers. Thus, many cancer categories and treatment regimens should be investigated in the context of the microbiome. Owing to the availability of metagenome sequencing and multiomics studies, analyses of species characterization, host genetic changes, and metabolic profile of gut microbiota have become feasible, which has facilitated an exponential knowledge gain about microbiota composition, taxonomic alterations, and host interactions during tumorigenesis. However, the complexity of the gut microbiota, with a plethora of uncharacterized host‐microbe, microbe‐microbe, and environmental interactions, still contributes to the challenge of advancing our knowledge of the microbiota‐cancer interactions. These interactions manifest in signaling relay, metabolism, immunity, tumor development, genetic instability, sensitivity to cancer chemotherapy and immunotherapy. This review summarizes current studies/molecular mechanisms regarding the association between the gut microbiota and the development of cancers, which provides insights into the therapeutic strategies that could be harnessed for cancer diagnosis, treatment, or prevention.

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Carcinogenesis mechanisms of Fusobacterium nucleatum

Cited by 138 publications

References 122 publications

Relationship of the mucosal microbiota to gastrointestinal inflammation and small cell intestinal lymphoma in cats

Relationship of the mucosal microbiota to gastrointestinal inflammation and small cell intestinal lymphoma in cats

The role of microbiota in the development of colorectal cancer

Harness the functions of gut microbiome in tumorigenesis for cancer treatment

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