Inhibition of miR-20 promotes proliferation and autophagy in articular chondrocytes by PI3K/AKT/mTOR signaling pathway.

Osteoarthritis is a common cause of functional deterioration in older adults and is an immense burden on the aging population. The molecular mechanism underlying the regulation of chondrocyte requires further elucidation, particularly with respect to the role of microRNAs. The aim of this study was to identify and characterize the expression of miR-20 in normal and OA chondrocytes, and to determine its role in OA pathogenesis. MiR-20 expression in cartilage specimens was examined in 30 patients with knee osteoarthritis and 30 traumatic amputees. The effect of miR-20 on chondrocyte was also investigated in chondrocyte cell line. Transfection with miR-20 mimic or inhibitor was employed to investigate the effect of miR-20 on chondrocyte proliferation and autophagy. Cell proliferation activity was detected by MTT assay and clone formation, cell autophagy were evaluated by monodansylcadaverine staining and GFP-LC3 fluorescence microscopy. Western blotting and immunohistochemical were utilized to detect expressions of autophagy markers (LC3, Beclin1 and p62) and of relevant proteins in the PI3K/AKT/mTOR signaling pathway. The results demonstrated that miR-20 inhibit chondrocyte proliferation and autophagy by targeting ATG10 via PI3K/AKT/mTOR signaling pathway. Our data suggest that miR-20 has an important role in the pathogenesis of osteoarthritis and is a potential therapeutic target.