Supplementary Material for: Research progress on lncRNA HCP5's regulation of hypertrophic scars by targeting miR-27b-3p
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https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Research_progress_on_lncRNA_HCP5_s_regulation_of_hypertrophic_scars_by_targeting_miR-27b-3p/30416734/1
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Introduction: Hypertrophic scars are common fibrotic disorders marked by fibroblast overgrowth and excessive extracellular matrix deposition, necessitating further research into their formation mechanisms to improve treatment outcomes. The study investigated the clinical significance and potential mechanisms of long noncoding RNA (lncRNA) HCP5 in the development of hypertrophic scars in human fibroblasts.
Methods: The study involved 63 patients to evaluate HCP5 expression through RT-qPCR. Cellular behaviors of human hypertrophic scar myofibroblasts (HSFs) were measured using CCK-8, Transwell, and flow cytometry assays. Targeting interactions between lncRNA HCP5 and miR-27b-3p were verified using a dual luciferase reporter assay.
Results: LncRNA HCP5 was significantly upregulated in hypertrophic scar tissue. More intriguingly, the silencing of lncRNA HCP5 led to a reduction in HSFs viability and migration, while simultaneously promoting apoptosis. Furthermore, miR-27b-3p was found to be downregulated and exhibited a negative correlation with lncRNA HCP5, both factors played crucial roles in regulating cellular behavior. In addition, the inhibition of miR-27b-3p may play a role in mitigating the effects induced by silenced lncRNA HCP5 on hypertrophic scars.
Conclusion: LncRNA HCP5 influenced the biological behavior of human hypertrophic scars by targeting miR-27b-3p.
引言:增生性瘢痕是一类常见的纤维化疾病,以成纤维细胞过度增殖及细胞外基质过度沉积为核心病理特征,目前仍需深入探究其发病机制以优化治疗效果。本研究旨在探讨长链非编码RNA(lncRNA)HCP5在人成纤维细胞参与的增生性瘢痕发生发展过程中的临床意义与潜在作用机制。
方法:本研究纳入63例患者,通过逆转录实时定量聚合酶链反应(RT-qPCR)检测HCP5的表达水平;采用细胞计数试剂盒-8(CCK-8)、Transwell及流式细胞术检测人增生性瘢痕肌成纤维细胞(HSFs)的细胞生物学行为;通过双荧光素酶报告基因实验验证lncRNA HCP5与miR-27b-3p之间的靶向结合关系。
结果:增生性瘢痕组织中lncRNA HCP5的表达显著上调。更值得关注的是,沉默lncRNA HCP5可降低HSFs的增殖活性与迁移能力,同时促进其凋亡。此外,miR-27b-3p在增生性瘢痕组织中表达下调,且与lncRNA HCP5呈负相关,二者均在调控细胞生物学行为中发挥关键作用。进一步研究发现,抑制miR-27b-3p可抵消lncRNA HCP5沉默对增生性瘢痕产生的调控效应。
结论:lncRNA HCP5可通过靶向调控miR-27b-3p,影响人增生性瘢痕的生物学行为。
提供机构:
Karger Publishers
创建时间:
2025-10-22



