Functional analysis of an oncogene SnoN as a target molecule to regulate progression of osteoarthritis.

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Osteoarthritis (OA) suppresses activity of patients, which conditions often lead patients to death. Loss of TGF-beta signaling in mice promotes hypertrophic maturation of chondrocytes in articular cartilage, the phenotype of OA. Among the downstream molecules of TGF-beta signaling, we focused on SnoN to examine its roles in chondrocyte maturation and pathogenesis of OA. SnoN was not expressed in human normal articular cartilage or immature chondrocytes of mice, while it was detected in human OA cartilage as well as in matured mouse chondrocytes. During BMP-induced chondrogenesis in vitro, SnoN suppressed BMP signaling to inhibit the chondrocyte maturation. Gain-of-function of SnoN mimicked the effects of TGF-beta application, therefore, SnoN was suggested to be a novel molecular target in treatment or prevention of OA.