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

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.