Mounting evidence has reported that microRNAs (miRNAs) play irreplaceable roles in the development ofkeloid fibrosis. miR-4417 has been reported to contribute to nickel chloride-promoted lung epithelial cellfibrogenesis and tumorigenesis. However, whether miR-4417 is involved in keloid fibrogenesis as well as itsunderlying mechanisms remain largely elusive. In this study, the expression levels of miR-4417 and CyclinD1in keloid tissues and fibroblasts were examined by qRT-PCR. Cell proliferation was determined by CCK assay.Western blot and flow cytometry were performed to evaluate cell apoptosis. Cell migration and invasion weremeasured by Transwell assay. Luciferase reporter assay was used to confirm the relationship between miR-4417 and CyclinD1. As a result, we found that miR-4417 was significantly down-regulated in keloid tissuesand fibroblasts. miR-4417 up-regulation led to the suppression of proliferation, migration, and invasion, whileinduced cell apoptosis in keloid fibroblasts. However, miR-4417 depletion exerted an opposite effect.CyclinD1 harbored the binding sites with miR-4417. Besides, the expression of CyclinD1 was evidentlydecreased in keloid tissues and fibroblasts. Meanwhile, miR-4417 was negatively correlated with CyclinD1 inkeloid tissue. The effect of CyclinD1 knockdown on keloid fibroblasts was similar to that of miR-4417overexpression. Furthermore, the elevated of CyclinD1 expression rescued the effect of miR-4417 up-regulationon keloid fibroblasts. miR-4417/CyclinD1 axis was required for cell proliferation, apoptosis, migration,and invasion in keloid fibroblasts. In conclusion, miR-4417 and CyclinD1 may be potential therapeutic targetsfor the treatment of keloid.