Wang Rui, Zhao Zigang, Zheng Liqiang, Xing Xiaojing, Ba Wei, Zhang Junfen, Huang Min, Zhu Wenwei, Liu Bing, Meng Xianfu, Bai Jia, Li Chengxin, Li Hengjin
Department of Dermatology, Chinese People's Liberation Army General Hospital, Medical College of the Chinese People's Liberation Army, Beijing 100853, P.R. China.
Exp Ther Med. 2017 Dec;14(6):6207-6212. doi: 10.3892/etm.2017.5323. Epub 2017 Oct 17.
Psoriasis is a chronic inflammatory disease of the skin for which an effective treatment strategy remains to be developed. Characteristics of psoriasis include an altered differentiation of keratinocytes and hyperplasia of the skin. The present study aimed to investigate the role served by miR-520a in psoriasis. The results demonstrated that miR-520a inhibited the proliferation of HaCaT cells. miR-520a directly regulated the mRNA and protein expression of its target gene, protein kinase B (AKT). The siRNA silencing of AKT expression in these cells was also evaluated. miRNA-520a repressed the proliferation and mitotic entry of HaCaT cells, and promoted cell apoptosis. AKT silencing suppressed the proliferation of HaCaT cells. These results suggest that miRNA-520a regulates the survival of HaCaT cells by inhibiting AKT expression. miRNA-520a and AKT may therefore be novel targets for the treatment of patients with psoriasis.
银屑病是一种慢性皮肤炎症性疾病，目前仍有待开发有效的治疗策略。银屑病的特征包括角质形成细胞分化改变和皮肤增生。本研究旨在探讨miR-520a在银屑病中的作用。结果表明，miR-520a抑制了HaCaT细胞的增殖。miR-520a直接调控其靶基因蛋白激酶B（AKT）的mRNA和蛋白表达。还评估了这些细胞中AKT表达的siRNA沉默情况。miRNA-520a抑制HaCaT细胞的增殖和有丝分裂进入，并促进细胞凋亡。AKT沉默抑制了HaCaT细胞的增殖。这些结果表明，miRNA-520a通过抑制AKT表达来调节HaCaT细胞的存活。因此，miRNA-520a和AKT可能是银屑病患者治疗的新靶点。
