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Abstract
The intestinal microbiota is potentially involved in the development of colorectal carcinoma via various mechanisms. Escherichia coli are commensal bacteria of the human gut microbiota, but some pathogenic strains have acquired the ability to induce chronic inflammation and/or produce toxins, such as cyclomodulin, which could participate in the carcinogenesis process. Here, we analyzed the E. coli population associated with mucosa of patients with colon cancer in relation to clinicopathologic characteristics. We assessed carcinogenic properties of a colon cancer-associated E. coli strain in multiple intestinal neoplasia (Min) mice. Mucosa-associated or internalized E. coli were quantified and characterized from tumors and mucosa of patients with colon cancer and the healthy mucosa of diverticulosis controls. Min mice were inoculated with a colon cancer-associated E. coli strain (11G5). The number of colonic polyps was evaluated at 7 weeks after infection. An increased level of mucosa-associated and internalized E. coli was observed in the tumors compared with normal tissue. A relationship between poor prognostic factors for colon cancer (tumor-node-metastasis stage) and colonization of mucosa by E. coli was observed. Pathogenic cyclomodulin-positive E. coli strains were more prevalent on mucosa of patients with stages III/IV than those with stage I colon cancer. Proliferative index and E. coli colonization level of the mucosa distant from the tumor significantly correlated. Min mice infected with the E. coli strain 11G5 displayed a marked increase in the number of visible colonic polyps compared with controls. These findings support that pathogenic E. coli could be a cofactor in pathogenesis of colorectal cancer.
Highlights
Colorectal cancer is the third most commonly diagnosed cancer worldwide and is responsible for more than 600,000 deaths every year
Pathogenic cyclomodulinpositive E. coli strains were more prevalent on mucosa of patients with stages III/IV than those with stage I colon cancer
multiple intestinal neoplasia (Min) mice infected with the E. coli strain 11G5 displayed a marked increase in the number of visible colonic polyps compared with controls
Summary
Colorectal cancer is the third most commonly diagnosed cancer worldwide and is responsible for more than 600,000 deaths every year. Colorectal carcinogenesis was first defined as a classic adenoma–carcinoma sequence by Fearon and Vogelstein in 1990 and several risk factors were identified to favor this tumoral development [3]. Approximately 20% of the global cancer burden can be linked to infectious agents [4, 5]. Bacteria and their related products could participate in initiation or progression of sporadic colon cancer by driving a variety of mechanisms, including the induction of proinflammatory and procarcinogenic pathways in epithelial cells, the production of genotoxins and reactive oxygen species, and the conversion of procarcinogenic dietary factors into carcinogens [6,7,8]. Various bacteria have been associated with carcinogenesis, including Streptococcus bovis, Enterococcus spp., Helicobacter pylori, the enterotoxigenic Bacteroides fragilis, and various www.aacrjournals.org
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