<i>Fusobacterium nucleatum</i> and colorectal cancer: A mechanistic overview

Goradel, Nasser Hashemi; Heidarzadeh, Siamak; Jahangiri, Samira; Farhood, Bagher; Mortezaee, Keywan; Khanlarkhani, Neda; Negahdari, Babak

doi:10.1002/jcp.27250

Cited by 140 publications

(109 citation statements)

References 100 publications

(156 reference statements)

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“…[7] The translocation of microbial pathogens leads to a series of immune responses, which promote carcinogenesis of host cells. [8][9][10][11] The estimated trillions of microbes that inhabit the human body establish a beneficial relationship with the host, but it is clear that disruption of this homeostasis (dysbiosis) may result in host disease, including inflammatory disorders and cancers. [12] However, whether there is a specific microbiome associated with MPE formation has not yet been determined.…”

Section: Introductionmentioning

confidence: 99%

Microbiome profile associated with malignant pleural effusion

et al. 2020

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Introduction There is ongoing research into the development of novel molecular markers that may complement fluid cytology malignant pleural effusion (MPE) diagnosis. In this exploratory pilot study, we hypothesized that there are distinct differences in the pleural fluid microbiome profile of malignant and non-malignant pleural diseases. Method From a prospectively enrolled pleural fluid biorepository, samples of MPE were included. Non-MPE effusion were included as comparators. 16S rRNA gene V4 region amplicon sequencing was performed. Exact Sequence Variants (ESVs) were used for diversity analyses. The Shannon and Richness indices of alpha diversity and UniFrac beta diversity measures were tested for significance using permutational multivariate analysis of variance. Analyses of Composition of Microbiome was used to identify differentially abundant bacterial ESVs between the groups controlled for multiple hypothesis testing. Results 38 patients with MPE and 9 with non-MPE were included. A subgroup of patients with metastatic adenocarcinoma histology were identified among MPE group (adenocarcinoma of lung origin (LA-MPE) = 11, breast origin (BA-MPE) = 11). MPE presented with significantly greater alpha diversity compared to non-MPE group. Within the MPE group, BA-MPE was more diverse compared to LA-MPE group. In multivariable analysis, ESVs belonging to family S24-7 and genera Allobaculum, Stenotrophomonas, and Epulopiscium were significantly enriched in the malignant group compared to the non-malignant group.

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Section: Introductionmentioning

confidence: 99%

Microbiome profile associated with malignant pleural effusion

et al. 2020

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“…Mechanisms underlying F. nucleatum ’s contribution to CRC development comprise immune modulation, miRNAs, bacteria metabolism and virulence factors, as already reviewed [ 147 , 148 ]. The Fusobacterium adhesin A (FadA), a bacterial cell surface adhesion component, is a protein virulence factor identified from F. nucleatum [ 149 , 150 ] that seems to be responsible for the carcinogenic effect of F. nucleatum .…”

Section: Other Bacterial Factors That May Influence Host Cell Tranmentioning

confidence: 99%

Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins?

Fiorentini¹,

Carlini

Germinario

et al. 2020

IJMS

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Accumulating evidence indicates that the human intestinal microbiota can contribute to the etiology of colorectal cancer. Triggering factors, including inflammation and bacterial infections, may favor the shift of the gut microbiota from a mutualistic to a pro-carcinogenic configuration. In this context, certain bacterial pathogens can exert a pro-tumoral activity by producing enzymatically-active protein toxins that either directly induce host cell DNA damage or interfere with essential host cell signaling pathways involved in cell proliferation, apoptosis, and inflammation. This review is focused on those toxins that, by mimicking carcinogens and cancer promoters, could represent a paradigm for bacterially induced carcinogenesis.

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“…e important mechanisms of Fusobacterium nucleatum involved in colorectal cancer are immune modulation (such as increased myeloid-derived inhibitory cells and natural killer-inhibiting receptors), virulence factors (such as FadA and Fap2), tRNA (such as miR-21), and bacterial metabolism [95].…”

Section: Fusobacterium Nucleatum and Colorectal Cancermentioning

confidence: 99%

“…Colorectal cancer is the fourth leading cause of cancer in worldwide, which occurs through several mechanisms including genetic, environment, life style, and role of bacterial chronic infections in development of colorectal cancer [ 94 ]. The important mechanisms of Fusobacterium nucleatum involved in colorectal cancer are immune modulation (such as increased myeloid-derived inhibitory cells and natural killer-inhibiting receptors), virulence factors (such as FadA and Fap2), tRNA (such as miR-21), and bacterial metabolism [ 95 ].…”

Section: Cancer Induced By Bacterial Infectionmentioning

confidence: 99%

Dual Role of Bacteria in Carcinoma: Stimulation and Inhibition

Al-Hilu

Al-Shujairi

2020

International Journal of Microbiology

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Although what unifies the carcinogenic microorganisms has not been determined by multiple studies, the role of bacteria in the development of neoplasms has not been properly elucidated. In this review, we discuss links between the bacterial species and cancer, with focus on immune responses for the stimulation of tumor cells such as induction of inflammation. Finally, we will describe the potential therapeutic strategies of bacteria on target tumors to improve treatment while mitigating adverse reactions. Cancer is a series of genetic changes that transform normal cells into tumor cells. These changes come from several reasons, including smoking, drinking alcohol, sunlight, exposure to chemical or physical factors, and finally chronic infection with microorganisms, including bacteria. In fact, bacterial infections are not carcinogenic, but recently it was discovered that the association between bacteria and cancer is through two mechanisms, the first stimulating chronic inflammation and the second producing carcinogenic metabolites. While bacteria are carcinogenic agents also, they have a dual role eliminating and removing tumor cells. However, the traditional cancer treatments that include chemotherapy, radiotherapy, surgery, and immunotherapy increase the chances of survival, and there are many side effects of these therapies, including the high toxicity of tissues and normal cells, could not penetrate the tumor cells, and resistance of these therapies by tumor cells. Therefore, the world has turned to an alternative solution, which is the use of genetically engineered microorganisms; thus, the use of living bacteria targeting cancerous cells is the unique option to overcome these challenges. Bacterial therapies, whether used alone or combination with chemotherapy, give a positive effect to treat multiple conditions of cancer. Also, bacteria can be used as vectors for drug, gene, or therapy, and this is a great step to treat cancer. Thus, we review the mechanisms underlying the interaction of the microbiota residents with cancer. Cancer-associated bacteria differ from those in healthy human and are linked with gene-expression profile. We also discuss how live bacteria interact with tumor microenvironments to induce tumor regression through colonization and spread. Finally, we provide past and ongoing clinical trials that include bacteria targeting tumors.

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Fusobacterium nucleatum and colorectal cancer: A mechanistic overview

Cited by 140 publications

References 100 publications

Microbiome profile associated with malignant pleural effusion

Microbiome profile associated with malignant pleural effusion

Gut Microbiota and Colon Cancer: A Role for Bacterial Protein Toxins?

Dual Role of Bacteria in Carcinoma: Stimulation and Inhibition

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