MiR‐20a has been reported as a key regulator to pro‐inflammatory factor release in fibroblast‐like synoviocytes (FLS), which caused rheumatoid arthritis (RA). However, the molecular mechanism of miR‐20a in RA remains to be further elucidated. This study aimed to investigate the roles of miR‐20a in RA pathology. RA (n = 24) and osteoarthritis (OA, n = 20) and normal healthy tissues (n = 16) were collected from operation. TargetScan and dual‐luciferase reporter were performed to predict and confirm the potential binding sites of miR‐20a on ADAM metallopeptidase domain 10 (ADAM10). Pearson's analysis was adopted to evaluate the correlation between miR‐20a and ADAM10 expression. It was found that MiR‐20a was downregulated in RA tissues, and overexpressed miR‐20a inhibited cell viability, migration and invasion, and the expression of inflammatory factors in RA‐FLS MH7A cells. ADAM10 was identified as the target gene of miR‐20a, and upregulation of ADAM10 reversed the inhibitory effects of miR‐20a. In conclusion, miR‐20a inhibits the progression of RA‐FLS as well as the inflammatory factor expression by targeting ADAM10.

中文翻译：

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MiR-20a通过靶向ADAM10抑制人关节炎成纤维细胞样滑膜细胞的进展和炎症因子的表达

据报道，MiR-20a 是成纤维细胞样滑膜细胞 (FLS) 中促炎因子释放的关键调节剂，导致类风湿性关节炎 (RA)。然而，miR-20a在RA中的分子机制仍有待进一步阐明。本研究旨在探讨 miR-20a 在 RA 病理学中的作用。从手术中收集RA（n = 24）和骨关节炎（OA，n = 20）和正常健康组织（n = 16）。使用 TargetScan 和双荧光素酶报告基因来预测和确认 miR-20a 在 ADAM 金属肽酶结构域 10 (ADAM10) 上的潜在结合位点。采用 Pearson 分析来评估 miR-20a 与 ADAM10 表达之间的相关性。研究发现 RA 组织中 MiR-20a 下调，过表达 miR-20a 抑制细胞活力、迁移和侵袭，以及炎症因子在 RA-FLS MH7A 细胞中的表达。ADAM10被确定为miR-20a的靶基因，ADAM10的上调逆转了miR-20a的抑制作用。总之，miR-20a 通过靶向 ADAM10 抑制 RA-FLS 的进展以及炎症因子的表达。