Regulation of MicroRNAs in Inflammation-Associated Colorectal Cancer: A Mechanistic Approach

Abstract

The development of colorectal cancer (CRC) is a multistage process. The inflammation of the colon as in inflammatory bowel disease (IBD) such as ulcerative colitis (UC) or Crohn's disease (CD) is often regarded as the initial trigger for the development of inflammation-associated CRC. Many cytokines such as tumor necrosis factor alpha (TNF-α) and interleukins (ILs) are known to exert proinflammatory actions, and inflammation initiates or promotes tumorigenesis of various cancers, including CRC, through differential regulation of microRNAs (miRNAs/miRs). miRNAs can be oncogenic miRNAs (oncomiRs) or anti-oncomiRs/tumor suppressor miRNAs, and they play key roles during colorectal carcinogenesis. However, the functions and molecular mechanisms of regulation of miRNAs involved in inflammation-associated CRC are still anecdotal and largely unknown. Consolidating the published results and offering perspective solutions to circumvent CRC, the current review is focused on the role of miRNAs and their regulation in the development of CRC. We have also discussed the model systems adapted by researchers to delineate the role of miRNAs in inflammation-associated CRC.

Keywords: Colorectal cancer (CRC); colitis-associated CRC (CAC); cytokines; inflammation; inflammation-associated CRC; inflammatory bowel disease (IBD); interleukin (IL); metastasis; microRNA (miRNA/miR); nuclear factor (NF) kappalightchain- enhancer of activated B cells (NFκB); tumor necrosis factor (TNF); ulcerative colitis (UC).