Abstract
The gut microbiota has emerged as an environmental contributor to colorectal cancer (CRC) in both animal models and human studies. It is now generally accepted that bacteria are ubiquitous colonizers of all exposed human body surfaces, including the entire alimentary tract (5). Recently, the concept that a normal bacterial microbiota is essential for the development of inflammation-induced carcinoma has emerged from studies of well-known colonic bacterial microbiota. This review explores the evidence for a role of fusobacteria, an anaerobic gram-negative bacterium that has repeatedly been detected at colorectal tumor sites in higher abundance than surrounding histologically normal tissue. Mechanistic studies provide insight on the interplay between fusobacteria, other gut microbiota, barrier functions, and host responses. Studies have shown that fusobacteria activate host inflammatory responses designed to protect against pathogens that promote tumor growth. We discuss how future research identifying the pathophysiology underlying fusobacteria colon colonization during colorectal cancer may lead to new therapeutic targets for cancer. Furthermore, disease-protective strategies suppressing tumor development by targeting the local tumor environment via bacteria represent another exciting avenue for researchers and are highlighted in this review.
Highlights
There are an estimated 142,820 new cases of colorectal cancer (CRC) annually in the United States, with over 50,000 deaths [1]
The observations of the active role of the gut microbiome in tumorigenesis have resulted in an energetic search for causative agents among normal flora bacteria
Studies of genetically deficient rodent models demonstrate an association between F. nucleatum (Fn) and CRC
Summary
There are an estimated 142,820 new cases of colorectal cancer (CRC) annually in the United States, with over 50,000 deaths [1]. Colorectal carcinomas are classified by etiology as inherited (e.g., hereditary nonpolyposis colorectal cancer due to genetic instability and familial adenomatous polyposis (FAP) coli due to a mutation in the adenomatous polyposis coli gene, APC), inflammatory (e.g., Crohn’s disease and ulcerative colitis), or sporadic [2]. Previous studies have established that consumption of red and processed meats, highly refined carbohydrates, and alcohol carry an increased risk of CRC [4]. It is generally accepted that bacteria are ubiquitous colonizers of the human body, including along the gastrointestinal tract [5]. These bacterial communities are established at birth, and a lifelong symbiotic relationship forms, with the human providing nutrients. The concept that normal bacterial microbiota plays a role in the development of inflammation-induced cancer has gained prominence from the considerable colonic microbiota literature
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