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长链非编码 RNA MIR181A2HG 通过 miR-223-3p/SOX6 轴抑制角质形成细胞增殖。

LncRNA MIR181A2HG inhibits keratinocytes proliferation through miR-223-3p/SOX6 axis.

机构信息

School of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin 541199, Guangxi, P.R. China.

Key Laboratory of Biochemistry and Molecular Biology (Guilin Medical University), Education Department of Guangxi Zhuang Autonomous Region, Guilin 541199, Guangxi, P.R. China.

出版信息

Aging (Albany NY). 2024 Jun 6;16(11):9846-9858. doi: 10.18632/aging.205902.

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.

摘要

背景

银屑病是一种复杂且反复发作的慢性炎症性皮肤病,角质形成细胞的异常增殖在银屑病的发病机制中起着关键作用。长链非编码 RNA(lncRNA)在调节细胞功能方面起着不可或缺的作用。本研究旨在探讨 lncRNA MIR181A2HG 对调节角质形成细胞增殖的潜在影响。

方法

使用 qRT-PCR 评估 MIR181A2HG 的表达水平和 KRT6、KRT16 和 SOX6 的 mRNA 水平。使用 CCK-8 和 EdU 测定法评估角质形成细胞的活力和增殖。通过流式细胞术进行细胞周期分析。应用双荧光素酶报告基因检测验证 MIR181A2HG/miR-223-3p/SOX6 之间的相互作用。通过 Western blot 分析检测蛋白水平。

结果

研究发现银屑病病变组织中 MIR181A2HG 的表达水平低于正常组织。MIR181A2HG 的过表达导致 HaCaT 角质形成细胞增殖受到抑制。MIR181A2HG 的敲低促进细胞增殖。双荧光素酶报告基因检测和挽救实验提供了 MIR181A2HG、SOX6 和 miR-223-3p 之间相互作用的证据。

结论

lncRNA MIR181A2HG 作为 miR-223-3p 的海绵,通过靶向 SOX6 调节角质形成细胞的增殖,表明 MIR181A2HG/miR-223-3p/SOX6 可能是银屑病的潜在诊断和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ad/11210253/fc6dd5158f18/aging-16-205902-g001.jpg

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