LncRNA SNHG1/miR-320b/CTNNB1轴在瘢痕疙瘩形成过程中调控成纤维细胞的集体迁移。

IF 1.6 4区 医学 Q3 OPHTHALMOLOGY
Qiaoling Li, Bowei Zhang, Jie Lu, Anqi Li, Qingbiao Wa
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引用次数: 0

摘要

背景:探讨长链非编码RNA (lncRNA)小核仁RNA宿主基因1 (SNHG1)表达对瘢痕疙瘩形成的调控分子机制。方法:检测瘢痕疙瘩患者皮肤组织中SNHG1、miR-320b、Catenin β 1 (CTNNB1)在瘢痕疙瘩组织与正常皮肤组织中的表达差异。以正常培养的人成纤维细胞为空白组(Blank),转染si-SNHG1,沉默SNHG1的表达。采用MTT法、Transwell室法、RT-qPCR、Western blot (WB)检测。发现SNHG1和miR-320b,以及miR-320b和CTNNB1是双荧光素酶报告基因(DLRG)策略的靶标。结果:与正常皮肤组织比较,瘢痕疙瘩组织中SNHG1、CTNNB1表达升高,miR-320b表达降低(P < 0.05)。与空白组相比,si-SNHG1组转移和攻击细胞数量减少,增殖活性降低,miR-320b表达升高,CTNNB1表达降低,Pro-Collagen I、Cyclin D1、VEGF、α-平滑肌肌动蛋白(α-SMA)、基质金属肽酶-2 (MMP-2)、MMP-9的相对表达量(RE)降低(P < 0.05)。结论:SNHG1可靶向调控miR-320b, miR-320b可靶向调控CTNNB1。减少SNHG1的表达可以阻止成纤维细胞的转移、攻击和增殖。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LncRNA SNHG1/miR-320b/CTNNB1 axis regulating the collective migration of fibroblasts in the formation of keloid.

Background: To explore the regulatory molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) expression on keloid formation.

Methods: The expression differences of SNHG1, miR-320b, and Catenin Beta 1 (CTNNB1) in keloid tissue and normal skin tissue of patients with keloid were detected. Normal cultured human fibroblasts were used as the Blank group (Blank) and then transfected with si-SNHG1 to silence SNHG1 expression. MTT assay, Transwell chamber assay, RT-qPCR, and Western blot (WB) were used. SNHG1 and miR-320b, as well as miR-320b and CTNNB1, were found to be targeted using the dual luciferase reporter gene (DLRG) strategy.

Results: As against normal skin tissue, SNHG1 and CTNNB1 were increased, while miR-320b was decreased in keloid tissue (P < 0.05). As against the Blank, there was a drop in the number of transferring and attacking cells, a decrease in the proliferative activity, an increase in the expression of miR-320b, a decrease in CTNNB1, and the relative expression (RE) of Pro-Collagen I, Cyclin D1, VEGF, α-smooth muscle actin (α-SMA), matrix metallopeptidase-2 (MMP-2), and MMP-9 was decreased in the si-SNHG1 group (AG) (P < 0.05).

Conclusion: SNHG1 could target and regulate miR-320b, and miR-320b could target and regulate CTNNB1. Fibroblast transfer, attack, and multiplication may all be prevented by reducing SNHG1 expression.

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来源期刊
CiteScore
3.30
自引率
6.20%
发文量
40
审稿时长
1 months
期刊介绍: Cutaneous and Ocular Toxicology is an international, peer-reviewed journal that covers all types of harm to cutaneous and ocular systems. Areas of particular interest include pharmaceutical and medical products; consumer, personal care, and household products; and issues in environmental and occupational exposures. In addition to original research papers, reviews and short communications are invited, as well as concise, relevant, and critical reviews of topics of contemporary significance.
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