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
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).
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