Mir31, a microRNA, plays diverse roles in post-transcriptional gene regulation. It is involved in multiple biological processes, such as wound healing, immune response regulation, and epithelial regeneration, and is associated with pathways like WNT and Hippo signaling. Its abnormal expression is linked to various diseases including periodontitis, inflammatory bowel diseases, and cancers [1-7].

In colitis mouse models, MIR31-knockout and conditional-knockout mice developed more severe colitis with increased immune responses compared to control mice. MIR31 reduced the inflammatory response in colon epithelium by preventing the expression of inflammatory cytokine receptors (Il7R and Il17RA) and signaling proteins (GP130), and also promoted epithelial regeneration by regulating the WNT and Hippo signaling pathways [1].

In vocal fold wound healing in rats, MIR31 expression increased after injury but decreased in the late stage, and it was strongly co-expressed with genes involved in collagen production, suggesting its role in VFWH [2].

In RKO colon cancer cells, treatment with kaempferol-3-O-glycoside inhibited the expression of miR31, along with oncogenes KRAS and c-MYC, while overexpressing tumor suppressor genes [3].

In BRAFV600E-associated thyroid carcinoma, miR-31 was identified as an onco-miR that promotes tumour progression, and its genetic knockout inhibited PTC progression and enhanced 131I uptake [4].

In conclusion, Mir31 has essential functions in processes like inflammation regulation, wound healing, and cancer-related mechanisms. The use of Mir31 knockout and conditional knockout mouse models has significantly contributed to understanding its role in diseases such as colitis and thyroid carcinoma, providing insights into potential therapeutic strategies for these conditions.