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XIST/let-7i/HMGA1 轴在口腔黏膜下纤维性变中维持肌成纤维细胞的活性。

XIST/let-7i/HMGA1 axis maintains myofibroblasts activities in oral submucous fibrosis.

机构信息

School of Dentistry, Chung Shan Medical University, Taichung 402, Taiwan; Department of Dentistry, Chung Shan Medical University Hospital, Taichung 402, Taiwan.

Department of Anatomy, School of Medicine, China Medical University, Taichung 404, Taiwan.

出版信息

Int J Biol Macromol. 2023 Mar 31;232:123400. doi: 10.1016/j.ijbiomac.2023.123400. Epub 2023 Jan 23.

Abstract

Long non-coding RNA XIST promotes the development of various types of head and neck cancers, but its role in the progression of precancerous oral submucous fibrosis (OSF) has not been determined yet. As such, we aimed to examine whether XIST implicates in the regulation of myofibroblast activation. Our results showed that the expression of XIST was upregulated in OSF tissues and fibrotic buccal mucosal fibroblasts (fBMFs), and the silencing of XIST downregulated several myofibroblasts features. We demonstrated that elevation of let-7i after inhibition of XIST may lead to reduced myofibroblast activation. On the contrary, overexpression of high mobility group AT-Hook 1 (HMGA1) following the suppression of let-7i may result in enhanced myofibroblast activities. Moreover, we showed that the suppressive effect of silencing of XIST on myofibroblasts hallmarks was reversed by let-7i inhibition or HMGA1 overexpression, suggesting the pro-fibrotic property of XIST was mediated by downregulation of let-7i and upregulation of HMGA1. These findings revealed that myofibroblast activation of fBMFs may attribute to the alteration of the XIST/let-7i/HMGA1 axis. Therapeutic approaches to target this axis may serve as a promising direction to ameliorate the malignant progression of OSF.

摘要

长链非编码 RNA XIST 促进了多种头颈部癌症的发展,但它在癌前口腔黏膜下纤维性变(OSF)进展中的作用尚未确定。因此,我们旨在研究 XIST 是否参与调节成肌纤维细胞的激活。我们的结果表明,XIST 在 OSF 组织和纤维化颊黏膜成纤维细胞(fBMFs)中表达上调,沉默 XIST 可下调几种成肌纤维细胞特征。我们证明,抑制 XIST 后 let-7i 的升高可能导致成肌纤维细胞激活减少。相反,抑制 let-7i 后高迁移率族蛋白 A1(HMGA1)的过表达可能导致成肌纤维细胞活性增强。此外,我们表明,沉默 XIST 对成肌纤维细胞特征的抑制作用可被 let-7i 抑制或 HMGA1 过表达逆转,表明 XIST 的促纤维化特性是通过下调 let-7i 和上调 HMGA1 介导的。这些发现表明,fBMFs 中的成肌纤维细胞激活可能归因于 XIST/let-7i/HMGA1 轴的改变。针对该轴的治疗方法可能成为改善 OSF 恶性进展的有前途的方向。

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