The role of gut microbiota in the pathogenesis of colorectal cancer

Zhu, Qian; Gao, Renyuan; Wu, Wen; Qin, Huanlong

doi:10.1007/s13277-013-0684-4

Cited by 181 publications

(151 citation statements)

References 115 publications

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“…Disruption of the homeostasis (both qualitatively and quantitatively) of the intestinal microflora could promote cancer through different ways, for example by altering the number, diversity, and stability of commensal bacteria or by the action of pathogens (i.e. Bacteroides fragilis) or conditional commensals (Terzic et al, 2010;Zhu et al, 2013). Over the last years, evidence for a role of microbiota and toll-like receptors, a type of pattern recognition receptors, in CRC is emerging and literature on the different potential mechanisms involved has been reviewed recently (Moossavi and Rezaei, 2013).…”

Section: Colorectal Cancermentioning

confidence: 99%

Mechanisms Linking Colorectal Cancer to the Consumption of (Processed) Red Meat: A Review

Demeyer

Mertens

Smet

et al. 2015

Critical Reviews in Food Science and Nutrition

150

103

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Colorectal cancer (CRC) is the third most commonly diagnosed cancer in the world. The vast majority of CRC cases have been linked to environmental causes rather than to heritable genetic changes. Over the last decades, epidemiological evidence linking the consumption of red and, more convincingly, of processed red meat to CRC has accumulated. In parallel, hypotheses on carcinogenic mechanisms underlying an association between CRC and the intake of red and processed red meat have been proposed and investigated in biological studies. The hypotheses that have received most attention until now include (1) the presence of polycyclic aromatic hydrocarbons and heterocyclic aromatic amines, two groups of compounds recognized as carcinogenic, (2) the enhancing effect of (nitrosyl)heme on the formation of carcinogenic N-nitroso compounds and lipid peroxidation. However, none of these hypotheses completely explains the link between red and processed red meat intake and the CRC risk. Consequently, scientists have proposed additional mechanisms or refined their hypotheses. This review first briefly summarizes the development of CRC followed by an indepth overview and critical discussion of the different potential carcinogenic mechanisms underlying the increased CRC risk associated with the consumption of red and processed red meat.

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Section: Colorectal Cancermentioning

confidence: 99%

Mechanisms Linking Colorectal Cancer to the Consumption of (Processed) Red Meat: A Review

Demeyer

Mertens

Smet

et al. 2015

Critical Reviews in Food Science and Nutrition

150

103

View full text Add to dashboard Cite

show abstract

“…2,3 In addition to these factors, gut microbiota dysbiosis has been reported in CRC patients. [4][5][6][7][8][9] Recent pyrosequencing analysis of CRC-associated bacterial microbiota has revealed dysbiosis with, in particular, overrepresentation of Fusobacterium and Bacteroides. [10][11][12][13][14] In addition, our group and others have shown that colonic adenomas, carcinomas, and the mucosa of CRC patients are abnormally colonized by Escherichia coli belonging to the B2 phylogroup, with a high prevalence of E. coli producing a genotoxin, termed colibactin, encoded by the pks genomic island.…”

mentioning

confidence: 99%

Intracellular colon cancer-associated Escherichia coli promote protumoral activities of human macrophages by inducing sustained COX-2 expression

Raisch

Rolhion

Dubois

et al. 2015

Laboratory Investigation

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Intestinal dysbiosis has been reported in patients with colorectal cancer, and there is a high prevalence of Escherichia coli belonging to B2 phylogroup and producing a genotoxin, termed colibactin. Macrophages are one of the predominant tumor-infiltrating immune cells supporting key processes in tumor progression by producing protumoral factors such as cyclooxygenase-2 (COX-2). Here, we investigated whether B2 E. coli colonizing colon tumors could influence protumoral activities of macrophages. In contrast to commensal or nonpathogenic E. coli strains that were efficiently and rapidly degraded by macrophages at 24 h after infection, colon cancer-associated E. coli were able to resist killing by human THP-1 macrophages, to replicate intracellularly, and to persist inside host cells until at least 72 h after infection. Significant increases in COX-2 expression were observed in macrophages infected with colon cancer E. coli compared with macrophages infected with commensal and nonpathogenic E. coli strains or uninfected cells at 72 h after infection. Induction of COX-2 expression required live bacteria and was not due to colibactin production, as similar COX-2 levels were observed in macrophages infected with the wild-type colon cancer-associated E. coli 11G5 strain or a clbQ mutant unable to produce colibactin. Treatment of macrophages with ofloxacin, an antibiotic with intracellular tropism, efficiently decreased the number of intracellular bacteria and suppressed bacteria-induced COX-2 expression. This study provides new insights into the understanding of how tumor-infiltrating bacteria could influence cancer progression through their interaction with immune cells. Manipulation of microbes associated with tumors could have a deep influence on the secretion of protumoral molecules by infiltrating macrophages. Colorectal cancer (CRC) is one of the most commonly diagnosed malignancies worldwide, making it the fourth most common cause of cancer deaths throughout the world. 1 CRC is a heterogeneous disease, including at least three major forms: hereditary, sporadic, and colitis-associated CRC. A large body of evidence indicates that genetic mutations, epigenetic changes, chronic inflammation, diet, and lifestyle deeply affect CRC onset. 2,3 In addition to these factors, gut microbiota dysbiosis has been reported in CRC patients. [4][5][6][7][8][9] Recent pyrosequencing analysis of CRC-associated bacterial microbiota has revealed dysbiosis with, in particular, overrepresentation of Fusobacterium and Bacteroides. [10][11][12][13][14] In addition, our group and others have shown that colonic adenomas, carcinomas, and the mucosa of CRC patients are abnormally colonized by Escherichia coli belonging to the B2 phylogroup, with a high prevalence of E. coli producing a genotoxin, termed colibactin, encoded by the pks genomic island. [15][16][17][18][19][20] It has been recently demonstrated that cells that survive infection with colibactin-producing E. coli display hallmarks of cellular senescence accompanied with productio...

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“…In the colon, these conjugates are activated or decojugated by pathogenic bacterial β-glucuronidase enzyme and regains carcinogenic potential [34]. A high level of fecal β-glucuronidase activity was found in colon cancer patients and also in individuals at higher risk for colon cancer [34] [35]. Lactobacillus bacteria reduced the activity of β-glucuronidase by 76.0% (Lb.…”

Section: Altering Intestinal Environmentmentioning

confidence: 99%

Chemopreventive Potential of Probiotics and Prebiotics

Sunkata¹,

Herring²,

Walker³

et al. 2014

FNS

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Utilization of probiotics and prebiotics in food products and in the diet supplemental form continues to gain interest because of their health benefits. Cancer is the leading cause of death and strategies for chemoprevention are important to reduce mortality and morbidity. Probiotics are gaining attention to use as preventive agents. Efficacy of their use as chemopreventive agents was established through research. This review focused on the mechanisms of prebiotics and probiotics action against cancer. Benefits of probiotics against cancer are attributed to competitive exclusion of pathogenic bacteria, direct physical binding to carcinogens, altering intestinal environment to modulate the production enzymes, antioxidant activity and immune modulation. Prebiotics are indigestible food components that could promote the growth of probiotics. Chemopreventive properties of prebiotics are due to their production of short chain fatty acids and enhancing the immunity of the host. Anticarcinogenic properties of pre-and probiotics result from a combination of events rather from a single event.

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The role of gut microbiota in the pathogenesis of colorectal cancer

Cited by 181 publications

References 115 publications

Mechanisms Linking Colorectal Cancer to the Consumption of (Processed) Red Meat: A Review

Mechanisms Linking Colorectal Cancer to the Consumption of (Processed) Red Meat: A Review

Intracellular colon cancer-associated Escherichia coli promote protumoral activities of human macrophages by inducing sustained COX-2 expression

Chemopreventive Potential of Probiotics and Prebiotics

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