MiR-223: Infection, inflammation and cancer

M. Haneklaus, M. Gerlic, L. A.J. O'Neill, S. L. Masters*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review


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, IKKα, Roquin and STAT3. With regard to cancer, validated targets include C/EBPβ, 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-κB 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.

Original languageEnglish
Pages (from-to)215-226
Number of pages12
JournalJournal of Internal Medicine
Issue number3
StatePublished - Sep 2013
Externally publishedYes


FundersFunder number
Seventh Framework Programme268155


    • Cancer
    • Infection
    • Inflammation
    • MiRNA-223


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