Qiaoling Li, Bowei Zhang, Jie Lu, Anqi Li, Qingbiao Wa
{"title":"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。","authors":"Qiaoling Li, Bowei Zhang, Jie Lu, Anqi Li, Qingbiao Wa","doi":"10.1080/15569527.2025.2496634","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>To explore the regulatory molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) expression on keloid formation.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>As against normal skin tissue, SNHG1 and CTNNB1 were increased, while miR-320b was decreased in keloid tissue (<i>P <</i> 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) (<i>P <</i> 0.05).</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":11023,"journal":{"name":"Cutaneous and Ocular Toxicology","volume":" ","pages":"1-8"},"PeriodicalIF":1.6000,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LncRNA SNHG1/miR-320b/CTNNB1 axis regulating the collective migration of fibroblasts in the formation of keloid.\",\"authors\":\"Qiaoling Li, Bowei Zhang, Jie Lu, Anqi Li, Qingbiao Wa\",\"doi\":\"10.1080/15569527.2025.2496634\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>To explore the regulatory molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) expression on keloid formation.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>As against normal skin tissue, SNHG1 and CTNNB1 were increased, while miR-320b was decreased in keloid tissue (<i>P <</i> 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) (<i>P <</i> 0.05).</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":11023,\"journal\":{\"name\":\"Cutaneous and Ocular Toxicology\",\"volume\":\" \",\"pages\":\"1-8\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2025-05-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cutaneous and Ocular Toxicology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/15569527.2025.2496634\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"OPHTHALMOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cutaneous and Ocular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15569527.2025.2496634","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"OPHTHALMOLOGY","Score":null,"Total":0}
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.
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.