Abstract

The function of microRNA-21-5p (miR-21) in fibroblast-like synoviocytes in RA was still unclear. In our study, we used tumor necrosis factor alpha (TNFα) (10ng/ml) to mimic RA-FLSs and we found that normal FLS stimulated with TNFα caused the increasing expression of miR-21, a disintegrin and metalloproteinase with thrombospondin motifs 5 and matrix metalloproteinase 3, which were in accord with RA-FLSs changes. Our data showed that miR-21 overexpression significantly increased cell invasion and decreased apoptosis in FLSs. Knockdown of miR-21 in FLSs causes the opposite result. However, miR-21 may not affect the proliferation of FLSs. Meanwhile, we showed that miR-21 activated the PI3K/AKT signaling pathway to participate in RA by inhibiting PTEN expression. Taken together, our results suggested that miR-21 may play a positive role in RA and may be a promising new therapeutic target for RA.

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