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<p>Hypertrophic scar (HS) is a proliferative disorder that occurs after skin injury and generally leads to disfigurement and impaired skin function in patients. This study aims to delve into the biological role of long intergenic non-protein coding RNA 1711 (LINC01711) in HS, thereby identifying novel therapeutic approaches for HS. HS tissues and corresponding normal tissues were obtained from 35 patients. The expression of LINC01711 was evaluated by qRT-PCR. The effect of LINC01711 knockdown on HS fibroblasts (HSFs) was measured by CCK-8 assay, migration assay, and apoptosis assay. The molecular mechanisms were investigated through bioinformatics analysis and dual-luciferase reporter assay. The impact of LINC01711 on the expression of extracellular matrix (ECM) deposition markers was measured using ELISA assay. LINC01711 was upregulated in HS tissues and positively correlated with disease severity. The silencing of LINC01711 induced the suppression of cell viability, migration, and the promotion of apoptosis in HSFs. LINC01711 negatively modulated microRNA-34a-5p (miR-34a-5p) expression. Suppression of miR-34a-5p reversed the biological function of LINC01711 knockdown in HSFs. Furthermore, LINC01711 modulated collagen type I alpha 1 chain (COL1A1), tissue inhibitor of metalloprotease-1 (TIMP1), and actin alpha 2 (Acta2) expression in HSFs mediated by miR-34a-5p. The results demonstrated that LINC01711 functioned as a regulatory factor in the proliferation, migration, apoptosis, and ECM deposition of HSFs mediated by miR-34a-5p.</p>

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LINC01711 modulates proliferation, migration, and extracellular matrix deposition of hypertrophic scar fibroblasts by targeting miR-34a-5p

  • 期刊论文

  • 发表日期：

    2025年4月25日

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  • Lun Pan,
  • Chengshuai Sun,
  • Hua Jin,
  • Shaocong Lv

摘要

Hypertrophic scar (HS) is a proliferative disorder that occurs after skin injury and generally leads to disfigurement and impaired skin function in patients. This study aims to delve into the biological role of long intergenic non-protein coding RNA 1711 (LINC01711) in HS, thereby identifying novel therapeutic approaches for HS. HS tissues and corresponding normal tissues were obtained from 35 patients. The expression of LINC01711 was evaluated by qRT-PCR. The effect of LINC01711 knockdown on HS fibroblasts (HSFs) was measured by CCK-8 assay, migration assay, and apoptosis assay. The molecular mechanisms were investigated through bioinformatics analysis and dual-luciferase reporter assay. The impact of LINC01711 on the expression of extracellular matrix (ECM) deposition markers was measured using ELISA assay. LINC01711 was upregulated in HS tissues and positively correlated with disease severity. The silencing of LINC01711 induced the suppression of cell viability, migration, and the promotion of apoptosis in HSFs. LINC01711 negatively modulated microRNA-34a-5p (miR-34a-5p) expression. Suppression of miR-34a-5p reversed the biological function of LINC01711 knockdown in HSFs. Furthermore, LINC01711 modulated collagen type I alpha 1 chain (COL1A1), tissue inhibitor of metalloprotease-1 (TIMP1), and actin alpha 2 (Acta2) expression in HSFs mediated by miR-34a-5p. The results demonstrated that LINC01711 functioned as a regulatory factor in the proliferation, migration, apoptosis, and ECM deposition of HSFs mediated by miR-34a-5p.