miR-223: infection, inflammation and cancer
- Author(s)
- Haneklaus, M; Gerlic, M; O'Neill, LAJ; Masters, SL;
- Details
- Publication Year 2013-09,Volume 274,Issue #3,Page 215-226
- Journal Title
- JOURNAL OF INTERNAL MEDICINE
- Publication Type
- Journal Article
- Abstract
- Expression of the microRNA miR-223 is deregulated during influenza or hepatitis B infection and in inflammatory bowel disease, type 2 diabetes, leukaemia and lymphoma. Although this may also be the result of the disease per se, increasing evidence suggests a role for miR-223 in limiting inflammation to prevent collateral damage during infection and in preventing oncogenic myeloid transformation. Validated targets for miR-223 that have effects on inflammation and infection include granzyme B, IKK alpha, Roquin and STAT3. With regard to cancer, validated targets include C/EBP beta, E2F1, FOXO1 and NFI-A. The effect of miR-223 on these targets has been documented individually; however, it is more likely that miR-223 affects multiple targets simultaneously for key processes where the microRNA is important. Such processes include haematopoietic cell differentiation, particularly towards the granulocyte lineage (where miR-223 is abundant) and as cells progress down the myeloid lineage (where miR-223 expression decreases). NF-kappa B and the NLRP3 inflammasome are important inflammatory mechanisms that are dampened by miR-223 in these cell types. The miRNA can also directly target viruses such as HIV, leading to synergistic effects during infection. Here we review the recent studies of miR-223 function to show how it modulates inflammation, infection and cancer development.
- Publisher
- WILEY-BLACKWELL
- Keywords
- cancer; infection; inflammation; miRNA-223
- Research Division(s)
- Inflammation
- Publisher's Version
- https://doi.org/10.1111/joim.12099
- Terms of Use/Rights Notice
- © 2013 The Association for the Publication of the Journal of Internal Medicine
Creation Date: 2013-09-01 12:00:00