Psoriasis is a common immune-mediated chronic inflammatory
skin disease characterized by abnormal keratinocyte proliferation, differentiation and apoptosis. However, the exact etiology and pathogenesis are still unclear. Evidence is rapidly accumulating for the role of
microRNAs in
psoriasis. It has been demonstrated that
Interleukin-22 (IL-22) plays vital role in T cell-mediated immune response by interacting with keratinocytes in the pathogenesis of
psoriasis. The aim of our study was to explore the possible functional role of miR-20a-3p in
psoriasis and in
IL-22 induced keratinocyte proliferation. Here, we found that miR-20a-3p was down-regulated in psoriatic lesions and in HaCaT cells (human keratinocyte cell line) treated by
IL-22 stimulation. Functional experiments showed that overexpression of miR-20a-3p in HaCaT cells suppressed proliferation and induced apoptosis while its knockdown promoted cell proliferation and reduces cell apoptosis. Mechanistically, SFMBT1 was identified as the direct target of miR-20a-3p by dual
luciferase reporter assay. SFMBT1 knockdown was demonstrated to inhibit cell growth and induced apoptosis, which was consistent with the function of miR-20a-3p upregulation in HaCaT cells. In addition, results of western blot analysis showed that miR-20a-3p upregulation or SFMBT1 knockdown changed the
protein expression levels of TGF-β1 and
survivin. Our findings suggest that miR-20a-3p play roles through targeting SFMBT1 and TGF-β1/
Survivin pathway in HaCaT cells, and loss of miR-20a-3p in
psoriasis may contribute to hyperproliferation and aberrant apoptosis of keratinocytes.