Abstract
PURPOSE: Hypertrophic scar (HS) is a common clinical disease during skin injury recovery. Although medicines have been listed for treatment, none are universally effective, and the details of the underlying molecular regulation are yet to be revealed. This research was aimed at exploring the clinical value of lncRNA PVT1 in HS formation and its potential mechanisms in human hyperplastic scar myofibroblasts (HSFs). PATIENTS AND METHODS: Fifty-seven HS patients were enrolled. RT-qPCR was conducted to examine the RNA levels of lncRNA PVT1, miR-29a-3p and STAT3. CCK-8, Transwell, and flow cytometry were used to analyze cell proliferation, migration, and apoptosis. The targeting relationship of PVT1/miR-29a-3p and miR-29a-3p/STAT3 was proved by the dual luciferase reporter. RESULTS: Relative expression of lncRNA PVT1 in human HS tissues was higher compared with normal tissues. LncRNA PVT1 silencing slowed proliferation and migration and accelerated apoptosis in human HSFs. miR-29a-3p was downregulated in human HS tissues, which was negatively correlated with PVT1 levels. LncRNA PVT1 was covalently bound to miR-29a-3p. miR-29a-3p played an important role in the proliferation, migration, and apoptosis of human HSFs. miR-29a-3p inhibitor rescued the negative influence of lncRNA PVT1 silencing on cells. STAT3 was covalently linked to miR-29a-3p. CONCLUSION: LncRNA PVT1 was a potential biomarker for HS and regulated the biological behavior of human HSFs via miR-29a-3p/STAT3.