Modulation of miR-155-5p signalling via 5-ASA for the prevention of high microsatellite instability: an in vitro study using human epithelial cell lines

J Physiol Biochem. 2024 Aug;80(3):573-583. doi: 10.1007/s13105-024-01033-y. Epub 2024 Jul 10.

Abstract

5-aminosalicylic acid (5-ASA) is a first-line treatment for maintaining colitis remission. It is a highly effective, safe, and well-tolerated drug with anti-inflammatory and chemo-preventive properties. While patients with primary sclerosing cholangitis (PSC) with concomitant ulcerative colitis are treated with 5-ASA, the molecular mechanisms underlying the drug's chemo-preventive effects are not entirely understood. We previously reported that bile acids and lipopolysaccharide-induced miR-155 expression was associated with downregulating mismatch repair (MMR) proteins in CACO-2 cell lines. Therefore, in this investigation, a set of in vitro functional studies was performed to show the possible mechanisms behind the epigenetic relationship between miR-155 and 5-ASA's prevention of high microsatellite instability (MSI-H). In transient transfection with miR-155Mimic, which behaves like endogenous miRNA, we confirmed the relationships between miR-155 and its target MMR in three human intestinal epithelial cell lines: CACO-2, NCM460D and HT-29. We have shown, for the first time, that 5-ASA modulates MLH1, MSH2, MSH6 in miR-155 transfected cells. These findings underline that chemoprotective 5-ASA therapy can effectively attenuate the expression of miR-155 and potentially prevent a development of MSI-H in a subset of colorectal cancers associated with PSC.

Keywords: Aminosalicylic acids; Mismatch repair genes; Primary sclerosing cholangitis; miR-155.

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Caco-2 Cells
  • DNA Mismatch Repair
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism
  • HT29 Cells
  • Humans
  • Mesalamine* / pharmacology
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Microsatellite Instability* / drug effects
  • MutL Protein Homolog 1 / genetics
  • MutL Protein Homolog 1 / metabolism
  • MutS Homolog 2 Protein / genetics
  • MutS Homolog 2 Protein / metabolism
  • Signal Transduction / drug effects

Substances

  • MicroRNAs
  • MIRN155 microRNA, human
  • Mesalamine
  • MSH2 protein, human
  • MutL Protein Homolog 1
  • MLH1 protein, human
  • MutS Homolog 2 Protein
  • Anti-Inflammatory Agents, Non-Steroidal
  • DNA-Binding Proteins