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.

Epistatic effect of TLR3 and cGAS‐STING‐IKKε‐TBK1‐IFN signaling variants on colorectal cancer risk

“…Moreover, chronic intestinal inflammation has long been recognized as a prominent CRC driver . Patients affected by inflammatory bowel diseases (IBD), such as Crohn's disease or ulcerative colitis, have been reported to have an increased risk of CRC development .…”

Gut microbes as future therapeutics in treating inflammatory and infectious diseases: Lessons from recent findings

“…Moreover, intra-abdominal infections, robust use of antibiotics leading to the alteration of gut microbial composition may work in concert for the incidence and progression of colorectal carcinoma, and extraintestinal cancers (breast and hepatocellular carcinoma) [109,111,[113][114][115][116][117] predominantly through the dysregulation of inflammatory and metabolic circuits. Several current studies that assessed beta diversity through 16S rRNA sequencing have illustrated structural differences amongst the gut microbiota, where samples belonging to different disease status (cancer, adenoma, or control/normal adjacent tissue) cluster in different two-dimensional spaces indicating the presence of dysbiosis [118][119][120]. Analysis of community diversity/ richness indices has also shown a significant reduction in the microbial diversity in the feces of colorectal patients in comparison to the healthy controls [119].…”

“…A recent investigation revealed that gut microbiota can efficiently prevent non-steroidal anti-inflammatory drugs (NSAIDs)-induced ulcers and erosions in the small intestine [251]. Similarly, understandings on the crosstalk amongst the gut microbes, barrier function, and the inflammatory responses have provided novel dimensions in targeting the pathology of colorectal cancer and colitis-associated cancer [118,240].…”

Metagenomic Approaches for Investigating the Role of the Microbiome in Gut Health and Inflammatory Diseases

“…Different from other kinds of cancer affecting the large bowel which are caused by point mutations in several genes that control cell proliferation, survival, differentiation and migration [60], CRC is mostly attributed to environmental factors and lifestyle such as high fat diet, alcohol, red meat, smoking, obesity, or lack of physical activity [56,85]. There are several studies showing a connection between inflammatory processes and carcinogenesis, although the contribution of immunological mechanisms and inflammation to malignancy of CRC, it is not fully elucidated [86][87][88].…”

“…Helicobacter pylori which well established in the development of stomach cancer since 1994 being classified as carcinogenic by the International Agency for Research on Cancer has also been pointed out as risk factor for CRC, as the infection leads to initial inflammatory response by stimulating IL-1β production, and consequently causing epithelium injury such as metaplasia [85]. In some studies, there was an indication of increased risk of colorectal adenomas by the presence of H. pylori due to hypergastrinemia; however, there is a controversy in other metagenomic studies that did not found correlation or even did not identify the presence of the pathogen in the analyzed samples [99].…”