Microbiome and cancer

Cullin, Nyssa; Antunes, Camila Azevedo; Straussman, Ravid; Stein‐Thoeringer, Christoph K.; Elinav, Eran

doi:10.1016/j.ccell.2021.08.006

Cited by 326 publications

(227 citation statements)

References 301 publications

(331 reference statements)

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“…For example, Helicobacter pylori can bind to gastric epithelial cells through the adhesin HopQ and carcinoembryonic antigen-related cell adhesion molecules (CEACAM) and the virulence factor CagA is directly injected into epithelial cells through type 4 secretion system (T4SS). CagA could ultimately activate the Wnt/β-catenin pathway, leading to cell turnover and apoptosis ( 51 ). Pathogenic Escherichia coli has a complete set of virulence factors and toxins related to pathogenicity, including secretory genetic poison colibactin.…”

Section: Potential Pathogenic Mechanisms Of Microbiota In Pcmentioning

confidence: 99%

“…Pathogenic Escherichia coli has a complete set of virulence factors and toxins related to pathogenicity, including secretory genetic poison colibactin. Once in the host cell, colibactin induces cross-links between DNA strands and double-strand DNA breaks ( 51 ). Pancreatic tissue could counter this malignant effect induced by the microbiota through an inflammatory response.…”

Section: Potential Pathogenic Mechanisms Of Microbiota In Pcmentioning

confidence: 99%

“…catenin pathway, leading to cell turnover and apoptosis(51). Pathogenic Escherichia coli has a complete set of virulence factors and toxins related to pathogenicity, including secretory genetic poison colibactin.…”

mentioning

confidence: 99%

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Association of the Microbiota and Pancreatic Cancer: Opportunities and Limitations

et al. 2022

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The human body is thoroughly colonized by a wide variety of microorganisms, termed microbiota. Pancreatic cancer, one of the most aggressive forms of cancer, is no exception. The microbiota of pancreatic cancer largely influences and even dominates the occurrence, development and outcome of pancreatic cancer in many ways. Studies have shown that microbiota could change the malignant phenotype and prognosis of pancreatic cancer by stimulating persistent inflammation, regulating the antitumor immune system, changing the tumor microenvironment and affecting cellular metabolism. This is why the association of the microbiota with pancreatic cancer is an emerging area of research that warrants further exploration. Herein, we investigated the potential microbial markers of pancreatic cancer, related research models, the mechanism of action of microbiota in pancreatic cancer, and pancreatic cancer-microbiota-related treatment.

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Section: Potential Pathogenic Mechanisms Of Microbiota In Pcmentioning

confidence: 99%

Section: Potential Pathogenic Mechanisms Of Microbiota In Pcmentioning

confidence: 99%

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Association of the Microbiota and Pancreatic Cancer: Opportunities and Limitations

et al. 2022

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“…However, this methodology has limitations in analytical output and data interpretation, and exhibits poor reproducibility due to chimera generation and variation in the regions of 16S rRNA amplified gene and reference databases [ 69 ]. Therefore, a full RNA sequencing using methods like shotgun metagenome sequencing could allow improved characterization of the gut microbiome at the species and strain level compared to 16S rRNA gene sequencing method [ 70 ].…”

Section: Expert Opinionmentioning

confidence: 99%

Microbiome in Chronic Kidney Disease (CKD): An Omics Perspective

Lohia

Vlahou

Zoidakis

2022

Toxins

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Chronic kidney disease (CKD) is predominant in 10% of the world’s adult population, and is increasingly considered a silent epidemic. Gut microbiota plays an essential role in maintaining host energy homeostasis and gut epithelial integrity. Alterations in gut microbiota composition, functions and, specifically, production of metabolites causing uremic toxicity are often associated with CKD onset and progression. Here, we present the latest omics (transcriptomics, proteomics and metabolomics) studies that explore the connection between CKD and gut microbiome. A review of the available literature using PubMed was performed using the keywords “microb*”, “kidney”, “proteom”, “metabolom” and “transcript” for the last 10 years, yielding a total of 155 publications. Following selection of the relevant studies (focusing on microbiome in CKD), a predominance of metabolomics (n = 12) over transcriptomics (n = 1) and proteomics (n = 6) analyses was observed. A consensus arises supporting the idea that the uremic toxins produced in the gut cause oxidative stress, inflammation and fibrosis in the kidney leading to CKD. Collectively, findings include an observed enrichment of Eggerthella lenta, Enterobacteriaceae and Clostridium spp., and a depletion in Bacteroides eggerthii, Roseburia faecis and Prevotella spp. occurring in CKD models. Bacterial species involved in butyrate production, indole synthesis and mucin degradation were also related to CKD. Consequently, strong links between CKD and gut microbial dysbiosis suggest potential therapeutic strategies to prevent CKD progression and portray the gut as a promising therapeutic target.

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“…Probiotics could regulate gut microbiota structure and composition, thus modulating occurrence and development of colon cancer 35,36 . The present studies suggested that the structure and abundance of gut microbiota were correlated with the development of colon cancer via administration for living or inactivated probiotics.…”

Section: In This Studymentioning

confidence: 99%

Commensal Lactobacillus Suppress Colon Tumorigenesis and Progression by Modulation of Sphingosine 1-Phosphate Signaling in Mice

Wang

et al. 2022

Preprint

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Background: Gut microbiota and their secreted metabolites influence the initiation, progression, and treatment responsiveness of colon cancer. Microbiota-based therapy regulated by probiotics has been considered as an effective strategy for prevention and therapeutic of colon cancer, whereas the antitumor mechanisms influenced by microbiota and their metabolites with intervention of probiotic remain further investigated.Results: Here, we investigated the preventive and therapeutic efficiency of commensal Lactobacillus in subcutaneous tumor models, and the underlying antitumor mechanism through the alteration of gut microbiota and their metabolites regulated by commensal Lactobacillus. Interestingly, we found that tumor formation rate in subcutaneous tumor models reduced 86.21% and 82.76%, in comparison to tumor controls when administrated with living or inactivated Lactobacillus (JY300-8 and JMR-01) for 20 days in advance. Subsequently, continuously oral administration for living or inactivated commensal Lactobacillus suppressed significantly the growth of tumor, and the tumor volumes declined 65.2% and 61.18%, respectively. Furthermore, microbiome and metabolome analyses revealed that commensal Lactobacillus suppressed colon tumorigenesis and progression through the modulation of gut microbiota and metabolites which included the down-regulation of secondary bile acids, sphingosine 1-phosphate (S1P) signaling in cancer and pyrimidine metabolism, as well as the production of anticarcinogenic compounds in tumor-bearing mice. Particularly, limitation the effects of S1P signaling via the modulation of sphingosine expression using probiotics, exerted antitumor efficiency.Conclusions: The work indicated the feasibility of using an effectively safe strategy to prevent the occurrence of colon cancer, and provided a potential therapeutic target for new therapeutics strategy via altering S1P signaling in cancer.

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Microbiome and cancer

Cited by 326 publications

References 301 publications

Association of the Microbiota and Pancreatic Cancer: Opportunities and Limitations

Association of the Microbiota and Pancreatic Cancer: Opportunities and Limitations

Microbiome in Chronic Kidney Disease (CKD): An Omics Perspective

Commensal Lactobacillus Suppress Colon Tumorigenesis and Progression by Modulation of Sphingosine 1-Phosphate Signaling in Mice

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