Skin pharmacology and physiology · 2025
Research Progress on LncRNA HCP5's Regulation of Hypertrophic Scars by Targeting MiR-27b-3p.
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He Jianping, Xie Lanzhe, Zhang Zhuo, Han Peng
Аннотация
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 quantitative real-time PCR. 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.
METHODS: The study involved 63 patients to evaluate HCP5 expression through quantitative real-time PCR. 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.