瘢痕疙瘩
基因敲除
成纤维细胞
活力测定
伤口愈合
癌症研究
纤维连接蛋白
基因沉默
免疫印迹
细胞生物学
小RNA
细胞迁移
分子生物学
细胞外基质
化学
细胞
生物
细胞培养
病理
免疫学
医学
生物化学
基因
遗传学
作者
Jingzhe Yang,Pingyang Deng,Yonggang Qi,Xinshu Feng,Hailing Wen,Chen Feng-ping
标识
DOI:10.1016/j.jss.2020.09.038
摘要
Background Keloid is a benign fibroproliferative tumor of the skin caused by abnormal wound healing process after skin injury. Long noncoding RNAs have been reported to be involved in the development of keloid. However, the role and mechanism of nuclear enriched abundant transcript 1 (NEAT1) in keloid are still unknown. Methods Quantitative real-time polymerase chain reaction was performed to detect the expression of NEAT1, miR-196b-5p, and fibroblast growth factor 2 (FGF2). Western blot was conducted to measure the levels of collagen I, α-smooth muscle actin, fibronectin, and FGF2. Cell Counting Kit-8 assay and transwell assay were used to evaluate cell viability and migration, respectively. Dual-luciferase reporter assay was conducted to verify the targeting relationship between miR-196b-5p and NEAT1 or FGF2. Results NEAT1 was increased and miR-196b-5p was decreased in keloid tissues and fibroblasts. NEAT1 knockdown or miR-196b-5p overexpression suppressed cell viability, migration, and extracellular matrix (ECM) component production in keloid fibroblasts. MiR-196 b-5p was a target of NEAT1, and NEAT1 overexpression reversed the effect of miR-196b-5p on keloid fibroblast progression. Moreover, we found that miR-196b-5p directly targeted FGF2. FGF2 knockdown suppressed keloid fibroblast viability, migration, and ECM protein production. FGF2 overexpression abolished the effect of miR-196b-5p overexpression on keloid fibroblast development. Conclusions NEAT1 silencing suppressed cell viability, migration, and ECM expression in keloid fibroblasts by regulating miR-196b-5p/FGF2 axis, indicating a promising strategy for keloid treatment.
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