Research Paper Volume 16, Issue 11 pp 9846—9858
LncRNA MIR181A2HG inhibits keratinocytes proliferation through miR-223-3p/SOX6 axis
- 1 School of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin 541199, Guangxi, P.R. China
- 2 Key Laboratory of Biochemistry and Molecular Biology (Guilin Medical University), Education Department of Guangxi Zhuang Autonomous Region, Guilin 541199, Guangxi, P.R. China
- 3 Department of Dermatology, Affiliated Hospital of Guilin Medical University, Guilin 541001, Guangxi, P.R. China
- 4 Department of Dermatology, The Second Affiliated Hospital of Guilin Medical University, Guilin 541199, Guangxi, P.R. China
Received: November 1, 2023 Accepted: May 3, 2024 Published: June 6, 2024
https://doi.org/10.18632/aging.205902How to Cite
Copyright: © 2024 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background: Psoriasis is a complex and recurrent chronic inflammatory skin disease, and the abnormal proliferation of keratinocytes plays a crucial role in the pathogenesis of psoriasis. Long non-coding RNAs (lncRNAs) play an indispensable role in regulating cellular functions. This research aims to explore the potential impact of lncRNA MIR181A2HG on the regulation of keratinocyte proliferation.
Methods: The expression level of MIR181A2HG and the mRNA level of KRT6, KRT16, and SOX6 were assessed using qRT-PCR. The viability and proliferation of keratinocytes were evaluated using CCK-8 and EdU assays. Cell cycle analysis was performed using flow cytometry. Dual-luciferase reporter assays were applied to test the interaction among MIR181A2HG/miR-223-3p/SOX6. Protein level was detected by Western blotting analysis.
Results: The findings indicated that psoriasis lesions tissue exhibited lower levels of MIR181A2HG expression compared to normal tissue. The overexpression of MIR181A2HG resulted in the inhibition of HaCaT keratinocytes proliferation. The knockdown of MIR181A2HG promoted cell proliferation. The dual-luciferase reporter assay and rescue experiments provided evidence of the interaction among MIR181A2HG, SOX6, and miR-223-3p.
Conclusions: The lncRNA MIR181A2HG functions as a miR-223-3p sponge targeting SOX6 to regulate the proliferation of keratinocytes, which suggested that MIR181A2HG/miR-223-3p/SOX6 might be potential diagnostic and therapeutic targets for psoriasis.