Downregulated SOX9 mediated by miR‑206 promoted cell apoptosis in Legg-Calvé-Perthes disease
- Junzhong Luo
- Jiuhui Han
- Yazhou Li
- Yuchang Liu
Published online on: November 8, 2017
Legg-Calvé-Perthes disease (LCPD) commonly onsets in adolescents, and threatens their health. However, the potential mechanism underlying LCPD remains unclear. MicroRNA (miR)‑206 and SRY‑box 9 (SOX9) serve an important role in chondrocytes; however, their role in LCPD remains ambiguous. In the present study, whether miR‑206 and SOX9 mediated cell apoptosis in dexamethasone (DEX)‑induced LCPD was investigated. The chondrocytes of the LCPD and normal control group were isolated from clinical tissues. Reverse transcription‑quantitative polymerase chain reaction was used to evaluate the expression of miR‑206 and SOX9 mRNA. Western blotting was used to measure the protein level of SOX9. A combination of Annexin V‑fluorescein isothiocyanate flow cytometry was used to assess cell apoptosis. The association between miR‑206 and SOX9 was detected using a luciferase reporter assay. miR‑206 was overexpressed while SOX9 was downregulated in chondrocytes treated with DEX obtained from patients with LCPD. miR‑206 targeted SOX9 to regulate its expression. Overexpression of miR‑206 promoted cell apoptosis in TC28, while it was reversed by SOX9 overexpression. TC28 cells pretreated with DEX significantly promoted cell apoptosis, while cells transfected with miR‑206 inhibitor significantly reversed the effect; however, downregulated SOX9 abolished the effects of miR‑206 inhibitor. SOX9 mediated by miR‑206 possibly contributed to the pathogenesis of LCPD. The results of the present study suggest that miR‑206 and SOX9 function as important therapeutic targets for the future of clinical therapy.