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NCK1反义RNA 1（NCK1-AS1）通过调控miR-137/NCK1轴在口腔黏膜中发挥促纤维化作用。

NCK1 antisense RNA 1 (NCK1-AS1) exerts pro-fibrosis property in oral mucosa through modulation of miR-137/NCK1 axis.

作者信息

Huang Yu-Feng, Wei Yu-Lei, Wang Shih-Min, Yang Po-Yu, Hsieh Pei-Ling, Yeh Jung-Chun, Liao Yi-Wen, Yu Cheng-Chia, Kuo Wan-Yin

机构信息

School of Dentistry, Chung Shan Medical University, Taichung, Taiwan.

Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan.

出版信息

J Dent Sci. 2025 Jan;20(1):632-638. doi: 10.1016/j.jds.2024.11.003. Epub 2024 Nov 14.

DOI:10.1016/j.jds.2024.11.003
PMID:39873098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11762667/
Abstract

BACKGROUND/PURPOSE: Oral submucous fibrosis (OSF) is a premalignant condition of the oral cavity, and its pathogenesis remains largely unknown. A multitude of non-coding RNAs are aberrantly expressed in OSF, and their implication for the development of OSF is a matter meriting investigation.

MATERIALS AND METHODS

The functional role of long non-coding RNA NCK1-AS1 in myofibroblast activation of fibrotic buccal mucosal fibroblasts (fBMFs) derived from OSF tissues was assessed. Wound healing, collagen gel contraction and transwell migration assays have been employed to assess the myofibroblast activities. In addition, a luciferase-based reporter assay was used to illustrate the potential mechanism underlying the regulation of NCK1-AS1 in myofibroblast activation.

RESULTS

Silencing of NCK1-AS1 markedly downregulated myofibroblast activation and the expression of fibrosis markers in fBMFs. Besides, we demonstrated that NCK1-AS1 directly interacted with microRNA-137 (miR-137) and was negatively correlated with it. Moreover, we found that NCK1 was a target of miR-137 and positively related to NCK1-AS1. Our results demonstrated that NCK1-AS1 may regulate myofibroblast activation by suppressing miR-137 and upregulating NCK1.

CONCLUSION

We showed that NCK1-AS1 acted as a sponge of miR-137 and titrated the suppressive effect of miR-137 on NCK1 to modulate myofibroblast activation in OSF condition.

摘要

背景/目的：口腔黏膜下纤维化（OSF）是一种口腔癌前病变，其发病机制在很大程度上仍不清楚。多种非编码RNA在OSF中异常表达，它们对OSF发生发展的影响值得研究。

材料与方法

评估长链非编码RNA NCK1-AS1在源自OSF组织的纤维化颊黏膜成纤维细胞（fBMFs）的肌成纤维细胞激活中的功能作用。采用伤口愈合、胶原凝胶收缩和Transwell迁移实验评估肌成纤维细胞活性。此外，基于荧光素酶的报告基因实验用于阐明NCK1-AS1在肌成纤维细胞激活中的潜在调控机制。

结果

沉默NCK1-AS1可显著下调fBMFs中肌成纤维细胞的激活以及纤维化标志物的表达。此外，我们证明NCK1-AS1直接与微小RNA-137（miR-137）相互作用，且与之呈负相关。而且，我们发现NCK1是miR-137的靶标，与NCK1-AS1呈正相关。我们的结果表明，NCK1-AS1可能通过抑制miR-137并上调NCK1来调节肌成纤维细胞的激活。

结论

我们表明NCK1-AS1作为miR-137的海绵，减弱miR-137对NCK1的抑制作用，从而在OSF条件下调节肌成纤维细胞的激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/883b02156130/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/795427c501ce/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/fbd3bc0e6596/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/8890c9d93c7d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/883b02156130/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/795427c501ce/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/fbd3bc0e6596/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/8890c9d93c7d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64d4/11762667/883b02156130/gr4.jpg

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本文引用的文献

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口腔黏膜下纤维性变中 Pi3k/Akt 通路和 VEGF 的表达及相关性。
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MiR-424/TGIF2-Mediated Pro-Fibrogenic Responses in Oral Submucous Fibrosis.miR-424/TGIF2 介导的口腔黏膜下纤维化的促纤维化反应。
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