Gut microbiota, inflammation and colorectal cancer

Abstract

Although genes contribute to colorectal cancer, the gut microbiota are an important player. Accumulating evidence suggests that chronic infection and the ensuing inflammation contributes to tumor initiation and tumor progression. A variety of bacterial species and tumor-promoting virulence mechanisms have been investigated. Significant advances have been made in understanding the composition and functional capabilities of the gut microbiota and its roles in cancer. In the current review, we discuss the novel roles of microbiota in the progression of colon cancer. Although microbiota technically include organisms other than bacteria e.g., viruses and fungi, this review will primarily focus on bacteria. We summarize epidemiological studies of human microbiome and colon cancer. We discuss the progress in the scientific understanding of the interplay between the gut microbiota, barrier function, and host responses in experimental models. Further, we discuss the potential application in prevention, diagnosis, and therapy of colon cancer by targeting microbiota. We discuss the challenges lie ahead and the future direction in studying gut microbiome in colon cancer to close the gap between the basic sciences and clinical application.

Keywords: Beta-catenin; Colon cancer; Cytokines; Dysbiosis; Epidemiologic; Gut barrier; Human microbiome; Inflammation.

Fig. 1

Working models of general mechanisms for bacteria – associated (or induced) colon cancer. Through enhancing toxic bacterial products, decreasing beneficial bacterial metabolites, disrupted tissue barriers, translocation of microbes, dysbiosis leads to abnormal immune activation, chronic inflammation, and hyperpreliferation that contribute to the colorectal cancer. The host factor, such as genetic defect, could enhance the dysbiosis along with the environment trigger and change of dietary.