A tiny but crucial player bridging microbes and colonic carcinogenesis

Colorectal cancer (CRC) is one of the most common malignancies in the world (1). The probability of suffering from CRC is approximately 4–5%, and the risk of developing CRC is associated with characteristics such as age, chronic disease history, and lifestyle (2). CRC is caused by mutations in oncogenes, tumor-suppressor genes, and genes related to DNA repair mechanisms. The underlying pathogenic mechanisms are threefold; namely, chromosomal instability (CIN), microsatellite instability (MSI), and CpG island methylator phenotype (CIMP). In CRC, common mutations, chromosomal changes, and translocations reportedly affect important intracellular signaling pathways [WNT, mitogen activated protein kinase (MAPK)/phosphoinositide 3-kinase (PI3K), transforming growth factor (TGF)-β, and TP53] (2). In addition to genetic mutations, alterations in non-coding RNAs, such as microRNAs, also contribute to carcinogenesis.