miR-320b Is Down-Regulated in Psoriasis and Modulates Keratinocyte Proliferation by Targeting AKT3

We investigated the molecular mechanisms underlying the role of miRNAs in the pathogenesis of psoriasis to discover novel potential diagnostic markers and treatment targets. We screened Chinese Han individuals using gene chip technology to identify differentially expressed miRNAs in the epidermal tissue of lesions from patients with psoriasis versus that from healthy controls. We also used bioinformatics methods and molecular biology experiments to predict and verify target genes and signaling pathways that may have an underlying role in normal human epidermal keratinocyte (NHEK) proliferation. Differentially expressed miRNAs were found in the epidermal tissue of lesions from patients with psoriasis; 45 were upregulated, and 71 were downregulated. Among them, miR-320b was significantly downregulated. Low miR-320b expression levels in NHEKs promoted cell proliferation. The luciferase assay results showed that AKT3 is a target gene of miR-320b. The protein phosphorylation levels of STAT3 and SAPK/JNK in the intracellular signaling pathway were significantly upregulated by miR-320b downregulation. Our findings indicate that miR-320b negatively regulates NHEK proliferation by targeting AKT3 to regulate the STAT3 and SAPK/JNK signaling pathways and might participate in the pathogenesis of psoriasis in Chinese Han populations. miR-320b may also be a novel diagnostic marker or therapeutic target for this disease.