دورية أكاديمية
miR-181a/b-5p negatively regulates keratinocytes proliferation by targeting MELK.
العنوان: | miR-181a/b-5p negatively regulates keratinocytes proliferation by targeting MELK. |
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المؤلفون: | Niu, Mutian, Li, Mingzhao, Fan, Xiaomei, Chen, Fangru, Wang, Mengjiao, Liu, Qingbo, Liang, Bin, Gan, Shaoqin, Mo, Zhijing, Gao, Jintao |
المصدر: | Arch Dermatol Res ; ISSN:1432-069X ; Volume:316 ; Issue:6 |
بيانات النشر: | Springer |
سنة النشر: | 2024 |
المجموعة: | PubMed Central (PMC) |
مصطلحات موضوعية: | Keratinocytes, MELK, Proliferation, miR-181a-5p, miR-181b-5p |
الوصف: | Accumulating evidence indicates that microRNAs (miRNAs) have a vital effect on the pathogenesis of psoriasis. This study is conducted to investigate the potential involvement of miR-181a-5p and miR-181b-5p in the proliferation of HaCaT keratinocytes. Cell viability and proliferation were evaluated respectively in this study using the CCK-8 and the 5-ethynyl-2'-deoxyuridine (EdU) assays. The expression of Maternal Embryonic Leucine Zipper Kinase (MELK) and Keratin 16 (KRT16) mRNA and protein in tissues and cells was assessed using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. The Luciferase reporter system analyzes the connection between miR-181a-5p/miR-181b-5p and MELK. The results showed that miR-181a/b-5p expression was downregulated in the psoriasis lesions and negatively regulated the proliferation of keratinocytes. MELK was directly targeted by miR-181a-5p/miR-181b-5p. In addition, HaCaT keratinocytes proliferation was inhibited by knockdown of MELK while promoted dramatically by MELK overexpression. Notably, miR-181a/b-5p mimics could attenuate the effects of MELK in keratinocytes. In conclusion, our research findings suggested miR-181a-5p and miR-181b-5p negatively regulate keratinocyte proliferation by targeting MELK, providing potential diagnostic biomarkers and therapeutic targets for psoriasis. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
العلاقة: | https://doi.org/10.1007/s00403-024-03081-2Test; https://pubmed.ncbi.nlm.nih.gov/38795158Test |
DOI: | 10.1007/s00403-024-03081-2 |
الإتاحة: | https://doi.org/10.1007/s00403-024-03081-2Test https://pubmed.ncbi.nlm.nih.gov/38795158Test |
حقوق: | © 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature. |
رقم الانضمام: | edsbas.A9D4903B |
قاعدة البيانات: | BASE |
DOI: | 10.1007/s00403-024-03081-2 |
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