Li Qiaoling, Zhang Bowei, Lu Jie, Li Anqi, Wa Qingbiao
Center of Medical Cosmetology, Chengdu Second People's Hospital, Chengdu, Sichuan Province, China.
Department of Vascular and Thyroid Surgery, Sichuan Provincial People's Hospital, Sichuan Academy of Medical Sciences, Chengdu, Sichuan Province, China.
Cutan Ocul Toxicol. 2025 Jun;44(2):191-198. doi: 10.1080/15569527.2025.2496634. Epub 2025 May 2.
To explore the regulatory molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) expression on keloid formation.
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.
As against normal skin tissue, SNHG1 and CTNNB1 were increased, while miR-320b was decreased in keloid tissue ( 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) ( 0.05).
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.
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。
检测瘢痕疙瘩患者瘢痕疙瘩组织和正常皮肤组织中SNHG1、miR-320b和连环蛋白β1（CTNNB1）的表达差异。将正常培养的人成纤维细胞作为空白组（Blank），然后用si-SNHG1转染以沉默SNHG1表达。采用MTT法、Transwell小室法、RT-qPCR和蛋白质免疫印迹法（WB）。使用双荧光素酶报告基因（DLRG）策略发现SNHG1与miR-320b以及miR-320b与CTNNB1之间存在靶向关系。
与正常皮肤组织相比，瘢痕疙瘩组织中SNHG1和CTNNB1升高，而miR-320b降低（P<0.05）。与空白组相比，si-SNHG1组（AG）中转移和侵袭细胞数量减少，增殖活性降低，miR-320b表达增加，CTNNB1降低，Ⅰ型前胶原、细胞周期蛋白D1、血管内皮生长因子、α-平滑肌肌动蛋白（α-SMA）、基质金属蛋白酶-2（MMP-2）和MMP-9的相对表达降低（P<0.05）。
SNHG1可靶向调控miR-320b，miR-320b可靶向调控CTNNB1。降低SNHG1表达可能会抑制成纤维细胞的转移、侵袭和增殖。
