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<p>Hypertrophic scars (HS) arise from abnormal wound healing characterized by excessive fibroblast proliferation, enhanced migration, and resistance to apoptosis. Although the long non-coding RNA GAS5 (LncRNA GAS5) has been implicated in several fibrotic disorders, its function in HS remains largely unclear. This study investigated whether GAS5 regulates fibroblast behavior through a competing endogenous RNA (ceRNA) mechanism involving miR-205. Human skin tissue fibroblasts (HSTFs) were transfected with a GAS5 overexpression plasmid (pcDNA-GAS5) or miR-205 mimics, and cell proliferation, migration, and apoptosis were evaluated using CCK-8, Transwell, and Western blot assays. The predicted GAS5–miR-205 interaction identified through ENCORI was validated by dual-luciferase reporter assays. GAS5 overexpression significantly enhanced fibroblast proliferation and migration while inhibiting apoptosis, whereas miR-205 promoted apoptosis. Luciferase assays confirmed direct binding between GAS5 and miR-205, and co-transfection experiments demonstrated that miR-205 attenuated the pro-proliferative and anti-apoptotic effects of GAS5. These findings suggest that LncRNA GAS5 regulates fibroblast activation by sponging miR-205 through a ceRNA mechanism. This regulatory axis may be involved in hypertrophic scar–related fibroblast activation and represents a potential therapeutic target for pathological fibrosis.</p>

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The LncRNA GAS5/miR-205 ceRNA axis regulates fibroblast activation and may contribute to hypertrophic scarring

  • 期刊论文

  • 发表日期：

    2026年6月18日

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  • Rui Guo,
  • Jingjing Gong,
  • Junxiu Liu,
  • Wenjuan Qu,
  • Wei Yang

摘要

Hypertrophic scars (HS) arise from abnormal wound healing characterized by excessive fibroblast proliferation, enhanced migration, and resistance to apoptosis. Although the long non-coding RNA GAS5 (LncRNA GAS5) has been implicated in several fibrotic disorders, its function in HS remains largely unclear. This study investigated whether GAS5 regulates fibroblast behavior through a competing endogenous RNA (ceRNA) mechanism involving miR-205. Human skin tissue fibroblasts (HSTFs) were transfected with a GAS5 overexpression plasmid (pcDNA-GAS5) or miR-205 mimics, and cell proliferation, migration, and apoptosis were evaluated using CCK-8, Transwell, and Western blot assays. The predicted GAS5–miR-205 interaction identified through ENCORI was validated by dual-luciferase reporter assays. GAS5 overexpression significantly enhanced fibroblast proliferation and migration while inhibiting apoptosis, whereas miR-205 promoted apoptosis. Luciferase assays confirmed direct binding between GAS5 and miR-205, and co-transfection experiments demonstrated that miR-205 attenuated the pro-proliferative and anti-apoptotic effects of GAS5. These findings suggest that LncRNA GAS5 regulates fibroblast activation by sponging miR-205 through a ceRNA mechanism. This regulatory axis may be involved in hypertrophic scar–related fibroblast activation and represents a potential therapeutic target for pathological fibrosis.