Ying-Xuan Chen

Abstract Fusobacterium nucleatum, a commensal microorganism and opportunistic pathogen (a pathobiont), has emerged as a key player in both local and systemic diseases. In humans, F. nucleatum is found in the oral microbiota, but under certain conditions, it can spread to other ecological niches within the body, such as the gut microbiota. Importantly, F. nucleatum has a pathogenic role in periodontal disease, inflammatory bowel disease and various cancers, particularly colorectal cancer. F.

Introduction Colorectal cancer (CRC) stands as the second most frequent cause of cancer-related deaths worldwide.1 Statins, a class of Food and Drug Administration (FDA)-approved 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, are widely used to manage hypercholesterolemia. Numerous epidemiological studies have demonstrated an association between statin use and improved survival outcomes in CRC patients.

Abstract Fusobacterium nucleatum can bind to host cells and potentiate intestinal tumorigenesis. Here we used a genome-wide screen to identify an adhesin, RadD, which facilitates the attachment of F. nucleatum to colorectal cancer (CRC) cells in vitro. RadD directly binds to CD147, a receptor overexpressed on CRC cell surfaces, which initiated a PI3K–AKT–NF–κB–MMP9 cascade, subsequently enhancing tumorigenesis in mice.