Affiliation:
1. Department of Dermatology and Venereology, People’s Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Clinical Research Center for Dermatologic Diseases, Xinjiang Key Laboratory of Dermatology Research (XJYS1707), Urumqi, China
Abstract
Objectives We investigated the effect and mechanism of miR-21-3p on the biological behavior of keratinocyte HaCaT cells. Methods HaCaT cells were transfected with miR-21-3p mimics and miR-21-3p inhibitor, respectively. Cell proliferation was detected by CCK-8, and apoptosis and cell cycle were analyzed by flow cytometry. The expression changes of Bax and Bcl-2 were measured with immunohistochemistry. The mRNA expressions of IL-17A and STAT3 were detected by real-time fluorescence quantitative PCR. Cytokeratin 17 protein was detected by Western blot. The relationship between miR-21-3p and STAT3 was verified by dual luciferase reporter gene assay. Results The miR-21-3p mimics significantly promoted the proliferation and cell cycle progression of HaCaT cells. However, miR-21-3p mimics significantly inhibited cell apoptosis, decreased Bax expression and increased Bcl-2 expression. Additionally, miR-21-3p mimics significantly increased the expressions of Cytokeratin 17 protein, IL-17A mRNA and STAT3 mRNA. Of note, the miR-21-3p inhibitor exhibited contrary effects to miR-21-3p mimics. Furthermore, STAT3 was a direct target of miR-21-3p. Conclusion miR-21-3p may promote the abnormal proliferation and inhibit apoptosis of HaCaT cells, possibly through regulating JAK/STAT pathway and the expression of Cytokeratin 17.
Funder
Natural Science Foundation of Xinjiang Uygur Autonomous Region
Subject
Immunology,Immunology and Allergy,General Medicine