Interaction of Exosomal MicroRNA and Oxidative Stress in the Pathogenesis of Colitis-Associated Cancer.

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  • Additional Information
    • Source:
      Publisher: IMR Press Country of Publication: Singapore NLM ID: 101612996 Publication Model: Print Cited Medium: Internet ISSN: 2768-6698 (Electronic) Linking ISSN: 27686698 NLM ISO Abbreviation: Front Biosci (Landmark Ed) Subsets: MEDLINE
    • Publication Information:
      Publication: 2022- : Singapore : IMR Press
      Original Publication: Searington, NY : Frontiers in Bioscience
    • Subject Terms:
    • Abstract:
      Colitis-associated cancer (CAC) is the most serious complication of inflammatory bowel disease. In recent years, the incidence of CAC has increased worldwide. Oxidative stress (OS) is involved in the development of CAC through oxidative damage to biomolecules or activation of inflammatory signaling pathways. Exosomes are extracellular vesicles that act as messengers to deliver signals and macromolecules to target cells, making them important mediators of intercellular communication and exchange of biologically active molecules between cells. MicroRNAs (miRNAs) carried by exosomes regulate the pro- and anti-inflammatory pathways of OS and play a key role in communication between OS and cancer cells. This review describes the correlation between OS and exosomal miRNAs with the goal of identifying a novel therapeutic method for CAC.
      Competing Interests: The authors declare no conflict of interest.
      (© 2024 The Author(s). Published by IMR Press.)
    • Grant Information:
      2024JC-YBMS-664 Shaanxi Province Key Research and Development Program; 2021TD15 The Innovation Team of Xi'an Medical University; 24YXYJ0143 Xi'an Science and Technology Plan Project
    • Contributed Indexing:
      Keywords: colitis-associated cancer; exosome microRNAs; oxidative stress
    • Accession Number:
      0 (MicroRNAs)
    • Publication Date:
      Date Created: 20240829 Date Completed: 20240829 Latest Revision: 20240829
    • Publication Date:
      20240902
    • Accession Number:
      10.31083/j.fbl2908276
    • Accession Number:
      39206897