Role of the long non‑coding RNA HOTAIR/miR‑126 axis in an in vitro psoriasis model
- Weifeng Zha
- Bo Guo
- Shuyue Chen
- Junwei Lu
- Yunyun Shan
Affiliations: Department of Dermatology, Third People's Hospital of Hangzhou, Hangzhou, Zhejiang 310009, P.R. China, Department of Dermatology, Tongxiang Dermatosis Prevention Institute, Tongxiang, Zhejiang 314500, P.R. China, Department of Acupuncture, Integrated Chinese and Western Medicine Hospital of Xihu, Hangzhou, Zhejiang 310030, P.R. China
- Published online on: March 1, 2021 https://doi.org/10.3892/etm.2021.9878
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Psoriasis is a T‑cell‑mediated inflammatory skin disease that is characterized by excessive keratinocyte proliferation and persistent skin inflammation. Accumulating evidence suggests that long non‑coding RNAs (lncRNAs) are dysregulated in a number of inflammatory conditions. In the present study, an in vitro psoriasis cell model was established. Human HaCaT keratinocytes were activated using the inflammatory factor IL‑22. Briefly, HaCaT cells were starved in serum‑free DMEM for 24 h and then stimulated with 100 ng/ml IL‑22 in serum‑free DMEM for 24 h. Previous research indicated that HOX transcript antisense RNA (HOTAIR) may participate in the development of psoriasis. First, reverse transcription‑quantitative PCR (RT‑qPCR) analysis was performed to detect HOTAIR expression. The results indicated that HOTAIR expression was reduced in IL‑22‑stimulated HaCaT cells. Subsequently, a dual‑luciferase reporter assay was performed to verify the binding site between HOTAIR and microRNA (miR)‑126. The RT‑qPCR results indicated that miR‑126 expression was increased in IL‑22‑stimulated HaCaT cells. Moreover, the effects of HOTAIR and miR‑126 on IL‑22‑stimulated HaCaT cell proliferation and apoptosis were assessed. HaCaT cells were transfected with control‑plasmid, HOTAIR‑plasmid, HOTAIR‑plasmid + mimic control or HOTAIR‑plasmid + miR‑126 mimic for 24 h. At 24 h post‑transfection, the cells were stimulated with 100 ng/ml IL‑22 for 24 h and experiments were conducted. IL‑22 induced cell proliferation and suppressed apoptosis. However, HOTAIR‑plasmid inhibited cell viability and induced apoptosis in IL‑22‑stimulated HaCaT cells. In addition, the western blotting results indicated that HOTAIR‑plasmid increased cleaved caspase‑3 expression and the cleaved caspase‑3/caspase‑3 ratio, whereas the HOTAIR‑plasmid‑mediated effects were reversed by miR‑126 mimic. Collectively, the results of the present study demonstrated that the lncRNA‑HOTAIR/miR‑126 axis may be implicated in the regulation of psoriasis progression and may serve as a potential therapeutic target for psoriasis.