长链非编码 RNA 核富集转录本 1 对瘢痕成纤维细胞增殖、凋亡和迁移的影响.

BACKGROUND: It has been elucidated that downregulation of nuclear enriched abundant transcript 1 (NEAT1) inhibits the progression of keloid fibroblasts, but the exact mechanism is not fully understood. OBJECTIVE: To investigate the influences of long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) on the proliferation, apoptosis and migration of keloid fibroblasts by regulating the miR-136-5p/ubiquitin-specific protease 4 (USP4) axis. METHODS: Keloid fibroblasts were divided into five groups: si-NC group, control check group, si-NEAT1 group, si-NEAT1+miR-136-5p inhibitor group, and si-NEAT1+inhibitor-NC group. qRT-PCR was performed to measure the expressions of NEAT1 and miR-136-5p; cell counting kit-8 assay and EDU staining were performed to measure cell proliferation; flow cytometry was performed to measure apoptosis; scratch-healing experiment was performed to measure cell migration; western blot assay was performed to measure the protein expressions of USP4, p27, Bax, matrix metalloproteinase-9, α-smooth muscle actin, and type I collagen α1 chain; dual-luciferase assay was performed to examine the relationship of NEAT1 with miR-136-5p as well as the relationship of miR-136-5p with USP4. RESULTS AND CONCLUSION: Compared with the si-NC group, the NEAT1 expression, absorbance value at 450 nm, percentage of EDU positive cells, scratchhealing rate, the protein expressions of USP4, matrix metalloproteinase-9, α-smooth muscle actin, and type I collagen α1 chain decreased in the si-NEAT1 group (P < 0.05), while the expression of miR-136-5p, apoptosis rate, and the protein expressions of p27 and Bax increased (P < 0.05). miR-136-5p inhibitor reversed the effect of silencing NEAT1 on the biological behavior of keloid fibroblasts. There was a targeted regulatory relationship between NEAT1 and miR-136-5p as well as between miR-136-5p and USP4. To conclude, silencing NEAT1 may inhibit the proliferation and migration of keloid fibroblasts and induce apoptosis by regulating the miR-136-5p/USP4 axis.. [ABSTRACT FROM AUTHOR]